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1.
AIM: To observe the expression of Snail1 and insulin-like growth factor-1 (IGF-1) in NRK-52E cells induced by high glucose, and to investigate the relationship of Snail1 and IGF-1 in the mechanism of epithelial to mesenchymal transition (EMT) in diabetic kidney disease (DKD).METHODS: The NRK-52E cells were treated with Snail1 siRNA and IGF-1 siRNA after cultured with high glucose medium for 72 h, and divided into control group, high glucose group, non-targeting (NT) siRNA group, Snail1 RNAi group and IGF-1 RNAi group. The cells were harvested at 48 h and 72 h. Real-time PCR was used to detect the mRNA expression of Snail1, IGF-1, E-cadherin and fibronectin (FN), and the protein levels were determined by immunofluorescence staining.RESULTS: Compared with control group, the expression of E-cadherin at mRNA and protein levels declined after stimulation with high glucose (P<0.01), while that of FN was elevated (P<0.01). Meanwhile, the mRNA and protein levels of Snail1 and IGF-1 were markedly increased (P<0.01).The expression of E-cadherin at mRNA and protein levels was improved in Snail1 RNAi group as compared with high glucose group(P<0.01), while that of FN, IGF-1 and Snail1 was significantly down-regulated (P<0.01). The same changes were observed in IGF-1 RNAi group (P<0.01). The protein expression of each factor in NT group had no significant change as compared with high glucose group (P>0.05). Pearson correlation analysis showed a close positive relationship between the expression of Snail1 and IGF-1 protein (r=0.852, P<0.01).CONCLUSION: Snail1 may facilitate DKD development by regulating IGF-1 in the process of EMT.  相似文献   

2.
AIM:To investigate the effect of combined treatment with gonadotropin-releasing hormone analogue (GnRHa) and growth hormone (GH) on the linear growth in mid- and late pubertal girls at great bone ages with central precocious puberty (CPP) or early and fast puberty (EFP), and to determine the relation between C-type natriuretic peptide (CNP) signaling pathway and the accelerative effect of GH on long bone growth in these girls. METHODS:Twenty-two girls were diagnosed as CPP or EFP, whose bone ages were older than 11.5 years with impaired predicted adult height (PAH), and divided into GnRHa treatment group (treated with GnRHa alone, slow-release of triptorelin 60~80 μg/kg every 4 weeks, im) and combined treatment group (treated with GnRHa and GH, 1 U/kg GH every week for 6~7 times, sc). The height, weight and pubertal stage were determined every 3 months. At the beginning and after 6 months of the treatment, the bone age was evaluated and the serum concentrations of amino-terminal pro-C-type natriuretic peptide (NTproCNP), insulin-like growth factor 1 (IGF-1) and procollagen type 1 amino-terminal propeptide (P1NP) were measured. Height velocity (HV), height SD score for bone age (HtSDSBA), PAH and the serum indexes mentioned above were compared at the beginning and the end of the treatment. RESULTS:After 6 months of the treatment, HV, ΔHtSDSBA and ΔPAH of the girls treated with GnRHa+GH were statistically higher than those of the girls given GnRHa alone (P<0.01). Serum concentrations of NTproCNP, P1NP and IGF-1 were not significantly different between the beginning and the end of the 6-month combined treatment. The girls treated with GnRHa alone showed a significant decrease in both serum NTproCNP and P1NP levels (P<0.05) and no significant change of serum IGF-1 level after 6 months of the treatment. CONCLUSION: In the CPP or EFP girls who are in mid- and late puberty and at great bone ages, the combined treatment with GnRHa and GH may accelerate linear growth and improve predicted adult height. This effect of GH is not attributed to the change of serum IGF-1 level, and may be related in part to the acceleration of CNP-mediated long bone growth.  相似文献   

3.
AIM: To study the effect of chronic hypoxic hypercapnia on expression of heme oxygenase-1 (HO-1). METHODS: Sprague-Dawley rats were randomly divided into three groups: control group(A),hypoxic hypercapnic group(B), hypoxic hypercapnia+hemin group(C). HO-1 and HO-1 mRNA were observed in pulmonary arterioles by the technique of immunohistochemistry and in situ hybridization. RESULTS: ① mPAP and weight ratio of right ventricle (RV) to left ventricle plus septum (LV+S) were significantly higher in rats of B group than those of A and C group (P<0.01). Differences of mCAP were not significant in three groups(P>0.05). ② Blood CO concentration was significantly higher in rats of B group than that of A group (P<0.01), it was much higher in C group than that of B group(P<0.01). ③ Light microscopy showed that vessel well area/total area (WA/TA), density of medial smooth muscle cell (SMC) and media thickness of pulmonary arterioles were much higher in rats of B group than those of A and C group (P<0.01). ④ The observation by electron microscopy showed proliferation of medial smooth muscle cells and collageous fibers of pulmonary arterioles in rats of B group, hemin could reverse the changes mentioned above. ⑤ HO-1 and HO-1 mRNA in pulmonary arterioles was significantly higher in rats of B group than those of A group(P<0.01), and they were significantly higher in rats of C group than those of B group (P<0.01). CONCLUSION: Expression of HO-1 mRNA and HO-1 in pulmonary arterioles was enhanced by hypoxic hypercapnia. Hemin partly inhibited pulmonary hypertension and pulmonary vessel remodeling by enhancing the expression of HO-1 mRNA and HO-1.  相似文献   

4.
AIM:To investigate the post-receptor mechanism of growth hormone (GH) resistance and insulin (INS) resistance and their relationship in non-catch-up growth rats born small for gestational age (NCU-SGA), based on the post-receptor signalling cross-talk between GH and INS at PI3K signaling pathway. METHODS:NCU-SGA rat model was developed by food restriction to pregnant dams. 4 weeks old male NCU-SGA rats were studied. Total and phosphate insulin receptor substrate-1(IRS-1) and its downstream signal Akt levels in liver tissue were measured by Western blotting or immunoprecipitation at baseline, post-stimulating of insulin, and pre-treatment with JAK2 (post-receptor signaling protein of GH) inhibitor AG490 then given insulin stimulation, respectively. RESULTS:(1) Expression levels of total and phosphate IRS-1: No difference between NCU-SGA rats and normal control was observed (P>0.05). (2) Expression levels of Akt : At baseline, Akt was already activated in NCU-SGA rats compared to no Akt activation in normal control rats. However, post- stimulating of insulin, the increase level of phosphate Akt in NCU- SGA rats was remarkably lower than that in control rats (P<0.01). When pre-treatment with JAK2 inhibitor to block GH signaling pathway, the impaired Akt activity was significantly restored (P<0.01), which suggested that the signaling of GH uncouples signal transduction from IRS-1 to Akt in NCU-SGA rats.CONCLUSION:Insulin resistance is related to impaired IRS-1-Akt signaling pathway in NCU-SGA rats. GH resistance mediates and aggrevates INS resistance by uncoupling signal transduction from IRS-1 to Akt via signaling cross-talk at post-receptor level between GH and INS. PI3K/Akt may be the major site for this uncoupling.  相似文献   

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6.
AIM: To investigate the effect of Ganoderma lucidum spores powder on the expression of insulin-like growth factor-1 (IGF-1), nuclear factor-κB (NF-κB) and apoptosis of nerve cells in rats with epilepsy established by pentetrazole. METHODS: The sub-eclampsia dosage of pentetrazole (PTZ) was used to make epilepsy model. Ganoderma lucidum spores powder group was given from stomach. The enduring time and latent period were recorded. The immune reactivity of IGF-1, NF-κB/P65 and apoptosis of nerve cells were measured with immunohistochemical staining and TUNEL method. RESULTS: In high power sight (×400), there were much more apoptosis cells in hippocampus and brain cortex of model group (18.80±2.13, 16.87±2.00) than those in control group (0.97±0.52, 0.58±0.25). The expressions of IGF-1, NF-κB in model group were higher than those in control group. Compared with model group, the latent period of Ganoderma lucidum spores powder group at the 17th, 21th, 25th days were longer (P<0.05, P<0.05, P<0.01, respectively).There were less apoptosis cells in hippocampus and brain cortex of Ganoderma lucidum spores powder group (12.30±2.46, 10.48±1.33) than those in model group. The expression of NF-κB/P65 in Ganoderma lucidum spores powder group was lower than that in model group, but the immune reactivity of IGF-1 increased more distinctly in Ganoderma lucidum spores powder group than that in model group. CONCLUSION: IGF-1, NF-κB and apoptosis of nerve cells may have play a role in occurrence and development of PTZ-induced epilepsy. Ganoderma lucidum spores powder can suppress expression of NF-κB strongly, and facilitate the immune reactivity of IGF-1, which may be one of the mechanisms by which Ganoderma lucidum spores powder restrains the apoptosis of nerve cells caused by epilepsy to prevent the damages of nerve cells.  相似文献   

7.
AIM: To observe the protective effect of human insulin-like growth factor 1 (hIGF-1) on rat skeletal myoblasts with ischemic/reperfusion injury. METHODS: Myoblasts were isolated from SD rats, cultured, purified, and transfected with plasmid pLghIGF-1SN or pLgGFPSN. The myoblasts were divided into insulin-like growth factor (IGF) group (myoblasts transfected with pLghIGF-1SN), green fluorescent protein (GFP) group (myoblasts transfected with pLgGFPSN), and control group (untransfected myoblasts). The expression of hIGF-1 in myoblasts was investigated by immunocytochemistry, RT-PCR and ELISA. The proliferation rate of myoblasts 14 days after transfection was detected. To observe the protective effect of IGF-1 gene on skeletal myoblasts with ischemic/reperfusion injury 7 days after transfection, the apoptotic myoblasts were detected by the method of in situ TdT-mediated dUTP nick end labeling (TUNEL). The expression of bax and bcl-2 mRNA was detected by RT-PCR, and the expression of caspase-3 was determined by Western blotting. RESULTS: The expression of hIGF-1 in myoblasts transfected with pLghIGF-1SN was detected by immunocytochemistry, RT-PCR and ELISA, but not in myoblasts transfected by pLgGFPSN and untransfected myoblasts. The proliferation rate of myoblasts in IGF group was higher than that in other groups (P<0.05). The results of RT-PCR showed that the expression of bax mRNA significantly decreased and bcl-2 mRNA significantly increased in IGF group compared with GFP group (P<0.05). The results of Western blotting showed that the expression of caspase-3 significantly decreased in IGF group compared with GFP group (P<0.05). CONCLUSION: The transfection of hIGF-1 gene mediated by a retroviral vector produces a protective effect in rat skeletal myoblasts with ischemic/reperfusion injury. The mechanisms may be associated with down-regulating the expression of Bax and caspase-3 and up-regulating Bcl-2 expression.  相似文献   

8.
AIM:To study the relationship between serum insulin-like growth factor- 1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3) levels, bone mineral density(BMD) and bone metabolic markers in postmenopausal women. METHODS:Serum IGF-1, IGFBP-3, osteocalcin(BGP), isomeric C-telopeptide of type I collagen (β-CTX), estradiol(E2), calcitonin(CT), parathormone(PTH), calcium (Ca), and phosphorus(P) were measured in 90 postmenopausal osteoporosis patients and 70 healthy postmenopausal women. BMD of lumbar vertebra and left femoral neck were determined by dual energy X-ray absorptiometry.RESULTS:BMD of lumbar vertebra and left femoral neck decreased significantly (P<0.01), serum IGF-1, IGFBP-3, E2, CT and BGP decreased significantly (P<0.01), serum β-CTX and PTH increased significantly in postmenopausal osteoporosis group (P<0.01). There were no significantly differences in serum Ca, P between two groups (P>0.05). BMD of lumbar vertebra and left femoral neck were positively correlated with serum IGF-1, IGFBP-3, E2, CT and BGP, but negatively correlated with β CTX and PTH. There were no correlation with serum Ca, P and BMD.CONCLUSION:Serum IGF-1, IGFBP-3, E2, CT, BGP, β-CTX and PTH level were correlated with BMD of lumbar vertebra and left femoral neck. These markers can be one of the valuable evidences for screening osteoporosis in postmenopausal women.  相似文献   

9.
AIM: To study the effect of dexamethasone (DEX) on the adrenomedullin (ADM) and its gene expression in lung tissue of asthmatic rats. METHODS: 30 healthy male SD rats were randomly divided into three groups (10 for each). The asthmatic model was established by ovalbumin inhalation and injection. The mRNA expression of ADM was examined by RT-PCR and the protein expression was detected by immunohistochemical method. The airway wall thickness, the airway smooth muscle (ASM) thickness and pulmonary tissue changes were observed under light microscope. RESULTS: The expression of ADM mRNA and protein in the asthma group A were higher than those in the control group(group C) (P<0.05), indicating that the moderate expression of ADM in asthmatic rat lung tissue is compensatory. The expression was significantly higher in DEX group (group B) than that in group A (P<0.01), indicating that DEX stimulated the expression of ADM mRNA and protein in lung tissue of asthmatic rats. CONCLUSION: The remarkable expression of ADM after the therapy of dexamethasone is one of its therapeutic mechanisms.  相似文献   

10.
AIM:To investigate the down-regulation of insulin-like growth factor tgpe 1 receptor(IGF-1R) on the migration and invasion abilities of human endometrial cancer cell HEC-1B. METHODS:The siRNAs targeting IGF-1R gene were synthesized, cloned into a lentivirus expression vector and transfected into endometrial cancer HEC-1B cells(HEC-1B-KD group). The control cells(without virus transfection, HEC-1B-CON group) and negative virus transfection control cells(HEC-1B-NC group) were also set up. The gene silencing effect of siRNA targeting IGF-1R was determined by real-time PCR and Western blotting at mRNA and protein levels,respectively. The proliferation rate was detected by colony formation assay. The cell migration and invasion abilities were determined by Transwell experiment. The mRNA levels of matrix metalloproteinase(MMP)-2 and MMP-9 were measured by real-time PCR. RESULTS:The mRNA and protein levels of IGF-1R in HEC-1B-KD cells were significantly reduced by 81% and 91.5%, respectively(P<0.05). In anchorage-dependent growth by colony formation assay, HEC-1B-KD cells showed much less colonies than HEC-1B-CON cells and HEC-1B-NC cells. Compared with the control cells, knockdown of IGF-1R in HEC-1B cells resulted in significant reduction of cell motility. Down-regulation of IGF-1R in HEC-1B cells also significantly reduced the invasion potential(P<0.05). Down-regulation of IGF-1R substantially reduced the expression of MMP-2 and MMP-9 compared with the control cells. CONCLUSION:Knockdown of IGF-1R reduces the migration and invasion abilities of human endometrial cancer cells in vitro accompanied with a decrease in MMP-2 and MMP-9 expression.  相似文献   

11.
AIM: To evaluate the effect of isinglass on chronic atrophic gastritis(CAG) in rats and its mechanism. METHODS: An animal model of CAG in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol/L sodium deoxycholate and 0.1% ammonia water was established in SD rats. Isinglass was used as preventive therapy while we were establishing CAG rat model. Finally all the rats were executed and pathologic changes of the gastric mucosa were studied by gross appearance and microscopy and serum epidermal growth factor (EFG) and growth hormone(GH) contents were tested. RESULTS: In each isinglass prevention group, inflammation grade of gastric antrum was less than that in model group (P<0.01) while the mean ratio of the thickness of gastric mucosal gland and muscularis mucosa (L1/L2), the number of gastric glands in 1 mm lengths of mucosal layer in longitudinal sections were much better than those in model group (P<0.01).They were very close to normal control group (P>0.05). The expression of proliferating cell nuclear antigen (PCNA) in gastric mucosa and serum EFG level were higher than those in model group (P<0.01, P<0.05), but serum GH content showed no different between isinglass prevention group and model group. CONCLUSION: Isinglass preventes the gastric mucosal atrophy in the CAG model. Its mechanism may be related to the effects of decreasing the gastric mucosal damage， promoting the cell proliferation and increasing of internal EFG secretion.  相似文献   

12.
AIM: To investigate the effect of simvastatin intervention on the changes of blood pressure, serum lipid fluctuation and aortic configuration induced by high-sodium and high-fat diet in rats. METHODS: Sixty adult male SD rats were randomly divided into 5 groups (n=12): control (N)group, high salt (S)group, high fat (F) group, high salt+ high fat (SF) group and high salt+high fat + simvastatin (T) group. After fed for 16 weeks, the rats were subject to determine blood pressures and serum concentrations of triglycerides (TG),total cholesterol(TC) and soluble CD40 ligand (sCD40L). The expression of CD40/CD40L in the root of ascending aorta was detected by immunohistochemical method. The thickness of intima media in the ascending aorta as well as the ratio of lumen area/total vascular area were measured and calculated after HE staining. RESULTS: In S group, F group and SF group, systolic blood pressure was significantly higher than that in N group (P<0.01). Systolic blood pressure in T group were slightly higher than that in N group with statistical significance and significantly lower than that in SF group. The serum concentrations of TG and TC in F group and SF group were significantly higher than those in N group and T group (P<0.01), and no significant difference among S group, N group and T group was observed. In S group, F group and SF group, the serum concentrations of sCD40L were higher than that in N group and T group (P<0.05), meanwhile that in SF group was also higher than that in S group and F group (P<0.05). However, no significant difference of sCD40L concentration between S group and F group as well as N group and T group was observed. The expression of CD40/CD40L in the ascending aorta in S group, F group and SF group was higher than that in N group and T group (P<0.05), and that in SF group was also higher than that in S group and F group (P<0.05).No significant difference of CD40/CD40L expression between S group and F group as well as N group and T group was observed. The thickness of intima media in S group, F group and SF group was significantly thicker than that in N group (P<0.01), and no significant difference of the intima media thickness between T group and N group was observed. The ratio of lumen area/total vascular area in S group, F group and SF group was smaller than that in N group (P<0.05), and no significant difference of the ratio between T group and N group was found. CONCLUSION: Feeding high-fat and high-salt diet leads to blood pressure elevation, induces atherosclerosis, increases serum concentration of sCD40L and enhances the expression of CD40/CD40L in arterial tissues. The combination of the stimuli has stronger effect than a single factor. Statins protect the arterial tissues against atherosclerosis by decreasing the level of serum sCD40L and inhibiting the arterial expression of CD40/CD40L.  相似文献   

13.
AIM：To explore the effect of advanced glycosylation end products (AGEs) on the function of human adipose-derived stem cells (hADSCs) in promoting wound healing. METHODS：hADSCs were isolated by conventional method in vitro and divided into control bovine serum albumin (BSA) group, low-dose AGE-BSA group and high-dose AGE-BSA group. The proliferation and migration of hADSCs with different treatments were determined by WST-8 assay and Transwell assay, respectively. In addition, the expression of vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), and insulin-like growth factor-1(IGF-1) at mRNA and protein levels was determined by real-time PCR and ELISA analysis. RESULTS：Compared with control group, the proliferation and migration abilities were significantly inhibited in the hADSCs of AGE-BSA group. The mRNA expression of VEGF, HGF and IGF-1 in AGE-BSA group was obviously lower than that in control group. The contents of VEGF, HGF and IGF-1 in hADSCs-conditioned me-dium in AGE-BSA group were also obviously lower than those in control group. CONCLUSION：AGEs alter the intrinsic properties of hADSCs and impair their functions in promoting wound healing, thus affecting the therapeutic potential of hADSCs in the treatment of diabetic ulcers.  相似文献   

14.
AIM: To investigate the effects of folic acid on the expression of monocyte chemoattractant protein-1 (MCP-1) in aorta of rats with hyperhomocysteinemia induced by ingestion of execess methionine (Met). METHODS: Thirty male SD rats ［(200±20） g］ were divided into 3 groups (n=10 for each group): control group (fed with normal diet), high Met group (fed with normal diet enriched by 1.7% Met) and Met plus folate group (fed with normal diet plus 1.7% Met and 0.006% folate). The animals were fed with different regiments for 45 days. Levels of total plasma homocysteine (Hcy) were detected. The expression of MCP-1 protein in aorta was detected by immunohistochemistry and Western blotting. RESULTS: The high-methionine diet resulted in a significant increase in plasma Hcy levels (P<0.01). Serum Hcy levels were significantly lower in rats fed with high-methionine plus folate-rich diet than that in rats fed with high-methionine diet (P<0.01). The expression of MCP-1 were higher in aorta of rats fed with high-methionine diet than those in control rats (46.41±4.23 vs 15.73±2.74, P<0.05). The expression of MCP-1 was significantly reduced in aorta of rats fed with high-methionine plus folate-rich diet compared with rats fed with high-methionine diet (23.12±4.40 vs 46.41±4.23, P<0.05). CONCLUSION: High methionine diet for 45 days is sufficient to induce hyperhomocysteinemia. Folate supplementation to the rats fed with the high-methenine diet prevents elevation of Hcy levels in blood, and reduces the expression of MCP-1 in aorta of rats with hyperhomocysteinemia.  相似文献   

15.
HE Li-feng  MA Li-kun 《园艺学报》2010,26(2):227-232
AIM: To investigate the effects and mechanisms of atorvastatin on myocardial fibrosis induced by aldosterone in SD rats. METHODS: Forty male uninephrectomized SD rats were limited to drink 1% NaCl water for 4 weeks and assigned to the follow groups: vehicle control rats (CON group); aldosterone treated rats (ALD group); spironolactone + aldosterone treated rats (SPI+ALD group); atorvastatin + aldosterone treated rats (ATO+ALD group). Blood pressure was measured by catheterization. Expression of platelet-derived growth factor (PDGF-A, PDGF-B), platelet-derived growth factor receptor (PDGFR-α, PDGFR-β) and ectodermal dysplasia-1 (ED-1) were analyzed by immunohistochemistry. Collagen volume fraction (CVF) and perivascular collagen area (PVCA) were analyzed by Sirius-Red staining. Myocardium osteopontin protein was detected by Western blotting analysis. RESULTS: Mean arterial blood pressure in ALD group, SPI+ALD group and ATO+ALD group was elevated, and significant difference was observed between the three groups and vehicle control group (P<0.01 or P<0.05). Myocardial fibrosis was observed in ALD group. Compared to other three groups, the index of CVF and PVCA was increased significantly (P<0.01 or P<0.05). No significant difference of the index of CVF and PVCA between ATO+ALD group and SPI+ALD group was observed (P>0.05). Compared to other groups, the levels of PDGF-A, PDGF-B, PDGFR-α, ED-1 and OPN in ALD group were significantly increased (P<0.01 or P<0.05). The levels of PDGF-A, PDGF-B, PDGFR-α and OPN were no significant difference between ATO+ALD group and SPI+ALD group (P<0.01 or P<0.05). However, the level of ED-1 in ATO+ALD group was significantly decreased compared to SPI+ALD group (P<0.05). No significant difference of PDGFR-β level among four groups was found (P>0.05). CONCLUSION: These results suggest that atorvastatin may attenuate myocardial fibrosis induced by aldosterone. The mechanisms concern with reduction of macrophage infiltration, expression of inflammatory cytokines OPN, partially inhibition of platelet-derived growth factor and its receptor expression.  相似文献   

16.
AIM:To study the effect of tissue kallikrein gene (HK) treatment on blood pressure in type 2 diabetic rats and its mechanism. METHODS:Male Wistar rats were injected with low dose streptozotocin and fed with diets enriched in fat and sugar to form type 2 diabetic model. Recombinant adeno-associated viral vectors (rAAV)-mediated HK gene (HK group) or LacZ gene (LacZ group) was introduced to the diabetic rats. The systolic blood pressure was measured every 2 weeks. The acetylcholine (Ach)-dependent vasodilation response, the synthesis of nitric oxide (NO), the expression of endothelin-1 (ET-1) and endothelin-A receptor (ETA-R) in the aorta were detected. RESULTS:(1) Systolic blood pressure was significantly higher in diabetic rats than that in normal control rats. In HK group, systolic blood pressure was significantly reduced within 2 weeks after injection with rAAV·HK, reached near normal levels at 4 weeks and kept until the experiments ended (16 weeks). (2) In LacZ group, Ach-dependent vasodilation response of isolated aorta was markedly decreased than that in HK group (P<0.01). (3) The concentration of NO in the aorta of HK group were significantly higher than those in LacZ group. The expression of ET-1 and ETA-R mRNA were significantly decreased in HK group compared with those in LacZ group (P<0.01). CONCLUSION:rAAV-mediated HK gene delivery efficiently lowed blood pressure and attenuated the endothelial function partly through increasing the concentration of NO and inhibiting the expression of ET-1 and ETA-R of aorta in type 2 diabetic rats.  相似文献   

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18.
AIM: To study the effects of Yangyu Tuji (YYTJ) on delayed healing wound of diabetic rats caused by streptozotocin (STZ). METHODS: SD male rats were randomly divided into control group (control), model group (model); and 3 different dose groups of YYTJ. 55 mg/kg STZ were given by intraperitoneal injection except for control group. After 30 days, a round skin of 1.6 cm diametre was excised on all dorsal back of rats. The healing time and healing rate were observed according to re-epithelization. The content of collagenⅠ and Ⅲ was observed by Picric acid-Sirius red staining , Matrix metalloproteinase-1, 13 (MMP-1, -13), tissue inhibitor of metalloproteinases-1 (TIMP-1) by immuno-histochemistry assay. All data were analyzed by IPP software. RESULTS: The healing time in each group treated with YYTJ was shorter than that in model group (P<0.01), and the healing rate was increased (P<0.01, P<0.05). Content of type I collagen, ratio of type Ⅰ and Ⅲ collagen of high and mid dose group were significantly higher than that in model group (P<0.01) at 3rd, 7th, 11th day. The expression of MMP-1, -13 of each groups were higher than that in model group at 7th day (P<0.01, P<0.05), and MMP-1 trend to equal with model group at 11th day. MMP-13 was significantly lower than that in model group at 11th day (P<0.01, P<0.05). TIMP-1 of each group of wound was higher than that in model group at 3rd, 7th, 11th day (P<0.01, P<0.05). The ratio of type Ⅰ and Ⅲ collagens in each group was lower than that in model group at 11th day (P<0.01). Ratio of MMP-13 and TIMP-1 of high dose group and mid dose group were higher than that in model group at 3rd and 7th day (P<0.01). The ratio of each group was lower than that in model group at 11th day (P<0.01). Meanwhile, ratio of MMP-13 and TIMP-1 of high dose group and mid dose group were lower than that of lower dose group (P<0.05). CONCLUSION: It is possible that YYTJ accelerates wound healing by increasing collagen content of type Ⅰ and Ⅲ, especially type Ⅰ, as well as improves collagen deposition by regulating the balance of MMP and TIMP.  相似文献   

19.
AIM：To explore the association between estrogen and C-type natriuretic peptide (CNP)-induced endochondral ossification in pubertal girls, and to investigate the relationship between CNP signaling pathway and the gonadotropin-releasing hormone analogue (GnRHa)-associated linear growth reduction in girls with idiopathic central precocious puberty (ICPP). METHODS：Serum levels of estradiol (E2), N-terminal propeptide of CNP (NT-proCNP), insulin-like growth factor 1 (IGF-1) and N-terminal mid-fragment of osteocalcin (N-MID OC) were measured in 56 healthy girls at different pubertal stages, and in 13 girls with ICPP at the beginning, the end of the 6th and 12th months of GnRHa treatment. Height velocity (HV) was also calculated. RESULTS：(1) Serum NT-proCNP, IGF-1, E2 and N-MID OC levels in the 56 healthy girls increased at early puberty compared with prepubertal levels (P<0.05 or P<0.01). Serum NT-proCNP level remained high at middle puberty and peaked at late puberty (P<0.05). Serum IGF-1 and E2 levels continued to increase at middle puberty (P<0.01) and peaked at late puberty (P<0.01). Serum N-MID OC level peaked at middle puberty (P<0.05) and decreased at late puberty (P<0.05). (2) The HV and serum levels of NT-proCNP and N-MID OC in the 13 ICPP girls decreased at the end of the 6th month of GnRHa treatment compared with those at the beginning of GnRHa treatment (P<0.05), and remained low at the end of the 12th month of GnRHa treatment. Serum IGF-1 level at the end of the 6th and 12th months of GnRHa treatment remained as the same as that at the beginning. Serum E2 returned to the prepubertal level after GnRHa treatment (P<0.05). CONCLUSION：Serum NT-proCNP level increases across female pubertal process and peaks at late puberty, in parallel with serum E2 and IGF-1 levels. Elevated estrogen in female puberty may be associated with CNP-mediated adolescent growth spurt. Serum NT-proCNP level in ICPP girls decreases during GnRHa treatment, in parallel with linear growth velocity and bone formation. Linear growth reduction in girls with ICPP treated with GnRHa is partly due to decreased CNP-mediated long bone growth after estrogen inhibition.  相似文献   

20.
AIM: To investigate the relationship between circulating insulin-like growth factor-1 (IGF-1) and hypertension patients with left ventricular hypertrophy (LVH). METHODS: Serum IGF-1 concentrations in 53 patients with essential hypertension and 16 healthy persons were measured by enzyme immunoassay (EIA). RESULTS: The results showed that serum IGF-1 concentration in essential hypertension was significantly higher than that in non-hypertension. Serum IGF-1 concentration in myocardial hypertrophy was significantly higher than that in myocardial non-hypertrophy (275．5±116．4 vs 203．8±82．9，P<0．01). There was positive correlation between serum IGF-1 and LVMI (r=0．45). 10 of 22 hypertension patients in pulse pressure ≤60 mmHg group were found to have myocardial hypertrophy, the ratio was 45%. Circulating IGF-1 concentration of patients with hypertension in suffering time ≥15 years is lower than that in suffering time <15 years. 20 of 31 hypertension patients in pulse pressure >60 mmHg were found to have myocardial hypertrophy, the ratio was 65%. There was no significant difference in serum IGF-1 concentration between two groups. CONCLUSION: ①These results indicated that circulating IGF-1 concentration was increased in essential hypertension, suggesting that circulating IGF-1 participates in the pathophysiological process of essential hypertension. ②Serum IGF-1 concentration in myocardial hypertrophy was significantly higher than that in myocardial non-hypertrophy. There was positive correlation between serum IGF-1 and LVMI, indicating that serum IGF-1 may promote myocardial hypertrophy. ③According to the suffering time result, the circulating IGF-1 in hypertension decreased significantly in the patients whose suffering time was less than 15 years. ④The hypertension patients with myocardial hypertrophy showed positive correlation with higher pulse pressure (>60 mmHg), indicating that the increase in pulse pressure participates in the course of myocardial hypertrophy. ⑤There was no significant correlation between pulse pressure and serum IGF-1 concentration, suggesting that different mechanisms are involved in the development of myocardial hypertrophy between pulse pressure and IGF-1.  相似文献   

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