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1.
AIM: To observe the effect of rosiglitazone on serum resistin level and to investigate the possible mechanism of glomerular sclerosis in type 2 diabetic rats. METHODS: Ten-week-old Wistar rats were divided into diabetic nephropathy (DN) group (10 cases) and DN+rosiglitazone group (10 cases). The other 10 Wistar rats were used as normal control group. Type 2 diabetic rats were induced by cutting the right kidney and injecting small dose (35 mg/kg) of streptozocin (STZ). Rosiglitazone group received rosiglitazone 10 mg·kg-1·d-1 while normal control group and DN group were fed with normal chow diet. After 20 weeks, vessel blood was collected for plasma IL-1, TNF-α and resistin assayed by ELISA. The serum levels of glucose, creatinine, urea nitrogen and microalbum of 24 h urine were also detected. The expression of TGF-β1 in glomerulus was examined by immunohistochemistry. Smad2 phosphatase activity was detected by Western blotting. RESULTS: The plasma IL-1, TNF-α, hs-CRP and resistin, and microalbum of 24 h urine in rosiglitazone group, were significantly lower than those in DN group while the serum level of glucose was not different from that in DN group. The expression of TGF-β1 and phosphorylated level of Smad2 were lower in rosiglitazone group than those in DN group. The degree of glomerular sclerosis in rosiglitazone group was obviously lighter than that in DN group. CONCLUSION: Rosiglitazone delays and ameliorates the development of diabetic glomerular sclerosis. The mechanism is possibly related to the modulation of resistin and other inflammatory factors. Anti-inflammation is a potential way for controlling diabetic nephropathy. 相似文献
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AIM: To study effect of benazepril (an ACE inhibitor) on expression of insulin receptor (IR) and its substrate-1 (IRS-1) protein in renal tissue cell membrane in diabetic rats. METHODS: The rats were randomly divided into following groups: control (n=6),streptozotocin induced diabetic (n=7) and diabetic treated with benazepril (n=7). Body weight, kidney weight and kidney weight/body weight were observed after 4 weeks of treatment. ACE activities in plasma, renal tissue were measured by the fluorimetric assay. The expressions of IR and IRS-1 protein were determined by Western blot analysis in renal tissue cell membrane. RESULTS: After 4 weeks of treatment,benazepril significantly ameliorated kidney hypertrophy in diabetic rats. ACE activities in plasma,renal tissue were reduced by approximately 92.00% and 88.77%,respectively. Western blot analysis showed that the expressions of IR and IRS-1 protein were increased by 2.1 and 1.5 folds in renal tissue cell membrane in diabetic rats. However, benazepril reduced expression of IR and IRS-1 protein by 45.74% and 47.66%, respectively. CONCLUSIONS: Increased the expression of IR and IRS-1 protein might be related to abnormally active glucose metabolism in diabetic rat kidney. Down-regulation of expression of IR and IRS-1 protein might be one of important machnisms of Benazepril nephroprotection on diabetic rats. 相似文献
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AIM: To explore the change of the amount of GLUT4 protein at the plasma membrane of the rat skeletal muscle after high-fat feeding. METHODS: The animals were divided into three groups (ten for each): group I: control; group II: high-fat feeding; group III: high-fat feeding + dietary treatment. The rat model of insulin resistance (IR) was made by feeding high-fat diet for eight weeks. And then insulin-resistant rats were fed with chow diet for 4 weeks. Fasting plasma glucose and fasting serum insulin levels were measured before and after dietary treatment, respectively. Insulin treatment was achieved by intraperitoneal injection of insulin (10 unit insulin per kg body weight) 15 minutes before killing the animals. The right hindlimb skeletal muscle was rapidly dissected. Then the expression of GLUT4 protein at the plasma membrane in all the animals was assessed with Western bloting. RESULTS: The GLUT4 content at the plasma membrane in high-fat-fed rat skeletal muscle was significantly lower (about 31%) than that in controls (P<0.01). Dietary treatment partly corrected fasting blood glucose [from(6.20±0.39)mmol/L to(5.78±0.74)mmol/L]and fasting serum insulin levels [from(17.19±1.93)mU/L to(11.68±1.28)mU/L] and increased the GLUT4 content at the plasma membrane by 1.14-fold in insulin-resistant rat skeletal muscle. CONCLUSION: High-fat feeding induces IR in Sprague-Dawley rats. The mechanism may be involved in decreased cell-surface level of GLUT4 through affecting intracellular insulin signaling and then decreasing GLUT4 trafficking. 相似文献
4.
AIM:To explore the expression of glucose transporter 4 (GLUT4) in the endometrium of rats with polycystic ovarian syndrom (PCOS) and evaluate the relationship between GLUT4 expression and insulin resistance (IR). METHODS:54 female SD rats of 85 days were randomized to control group (n=20), PCOS model group (n=17) and metformin treatment group (n=17). The rats in the latter two groups were induced by Poretsky’s method for PCOS model, followed by placebo or metformin, respectively. After 14 days of treatment, the rats were sacrificed and the expression of GLUT4 in endometrium was detected by ElivisionTM Plus two steps immunohistochemical staining. RESULTS:The expression of GLUT4 and insulin receptor(INS-R) proteins of endometrial glandulan epitheliu in PCOS rats were significantly lower (P<0.01,P<0.05) than those in control group, however, the expression of insulin(INS) protein in PCOS rats was higher than that in control group (P<0.01). The expression of GLUT4 in the treatment group increased (P<0.01), but was still lower than that in control group (P<0.01). However, compared with PCOS group, the expression of INS protein was decreased (P<0.05), but was still higher than that in control group (P<0.05). There was no GLUT4 expression in interstitial cells in endometrium, and the changes of the expressions of INS and INS-R proteins in those cells were similar with those in glandulan epitheliu. CONCLUSION:The decrease in GLUT4 expression of endometrium in PCOS rats is related with endometrial insulin resistance. 相似文献
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AIM: To explore the mechanism of 3-nitropropionic acid (3-NPA) preconditioning that induces cerebral ischemic tolerance in rats by affecting the expression of brain-type glucose transporters (GLUT1 and GLUT3) at mRNA and protein levels in cerebral tissues.METHODS: The male SD rats were used in the experiments and divided randomly into sham operation group (sham group, n=4), control group of 3-NPA preconditioning (3-NPA group, n=4), cerebral ischemia group (M group, n=16) and 3-NPA preconditioning group (IPC group, n=16). M group and IPC group were further divided into 4 subgroups according to the different reperfusion time(4 h, 12 h, 24 h and 48 h). All rats were killed at the corresponding time points. The cerebral tissues in the ischemic side (left) and coronal intermediate 1/3 of cortex were collected. The protein levels and mRNA expression of GLUT1 and GLUT3 were determined by Western blotting and RT-PCR. RESULTS: Compared with M group, the ischemic reperfusion and 3-NPA preconditioning induced the upregulation of GLUT1 and GLUT3 at protein levels with significant differences (F=5.848, P<0.05 and F=6.295, P<0.05, respectively), especially after ischemia-reperfusion for 48 h. The mRNA expression of GLUT1 in IPC group began to increase at 4 h, peaked at 48 h after reperfusion, with significant difference as compared to M group at the corresponding reperfusion time points in each group or sham group. In contrast, the mRNA expression of GLUT3 in IPC group increased at 24 h, and was the highest at 48 h as compared to cerebral ischemia group at the corresponding reperfusion time points or sham group.CONCLUSION: 3-NPA preconditioning increases the expression of GLUT1 and GLUT3 at protein and mRNA levels to maintain the energy supply in brain tissues, indicating a cerebral protective mechanism. 相似文献
6.
LIU Yi WANG Dong-hua DENG Xiao-yan LV Li-qun SHENG Hui YIN Jie XIAO Wei GONG Cheng 《园艺学报》2008,24(8):1620-1624
AIM: To explore the effect of rosiglitazone on ovarian insulin resistance in polycystic ovarian syndrome (PCOS) by determining the tyrosine phosphorylation and protein expression of insulin receptor substrate 1 and 2 (IRS-1, IRS-2) in ovarian luteinizing granulosa cells from patients with PCOS. METHODS: Cultured luteinizing granulosa cells from PCOS (n=11) and normal ovulatory (as control, n=15) were obtained in the process of IVF. By treating with different concentrations of insulin for 48 h, the mRNA expressions of insulin receptor substrates (IRS-1, IRS-2) in ovarian luteinizing granulose cells were assessed by semi-quantitative RT-PCR. The protein and phosphorylation expressions of insulin receptor substrates (IRS-1, IRS-2) in ovarian luteinizing granulose cells were analyzed by Western blotting and immunoprecipitation. RESULTS: (1) As compared with control group, luteinizing granulose cells in PCOS patients had higher IRS-1mRNA expression and protein content(P<0.05), but lower IRS-2mRNA expression and protein content (P<0.05). The phosphorylation expressions of IRS-1 and IRS-2 were significantly lower (P<0.05) at the basic state. (2) Rosiglitazone corrected the abnormal protein expression and improved the tyrosine phosphorylation of insulin receptor substrate 1 and 2 (IRS-1, IRS-2) in ovarian luteinizing granulosa cells from patients with PCOS. (3) Rosiglitazone had no effect on the tyrosine phosphorylation and protein expression of insulin receptor substrate 1 and 2 (IRS-1, IRS-2) in ovarian luteinizing granulosa cells from normal ovulatory control. CONCLUSION: (1) There is a selective insulin resistance in ovarian luteinizing granulosa cells from patients with PCOS, the reason may be related to abnormal tyrosine phosphorylation and protein expression of insulin receptor substrates. (2) Rosiglitazone improves ovarian function of PCOS, the reason may be related to correct the abnormal protein expression and improve the tyrosine phosphorylation of insulin receptor substrates in ovarian luteinizing granulosa cells. 相似文献
7.
AIM: To investigate the effect of taurine on the expression of glucose transporter 1 (GLUT1) and transporter 3 (GLUT3) in rat brain with diffused brain injury (DBI).METHODS: Sixty-four male Sprague-Dawley rats were randomly divided into 4 groups: sham-operated group, DBI group, low-dose taurine group (200 mg/kg, ig) and high-dose taurine group (300 mg/kg, ig).After fed with the corresponding drugs for 7 days, the animal model of DBI was made, and the rats were executed 24 h after DBI.The expression of GLUT1 and GLUT3 in the brain was detected by the methods of immunohistochemistry and Western blotting.The pathomorphological changes of the cerebral cortex were observed under electron microscope.RESULTS: The expression of GLUT1 was detected in capillary vascular endothelial cells in each group, and cytoplasm-positive cells or the cells with buffy membrane were observed.No significant difference of the GLUT1 expression in brain tissues between DBI group and sham-operated group was detected.Compared with DBI group, the expression of GLUT1 in the brain tissues were significantly increased in low-and high-dose taurine groups (P<0.01).The expression of GLUT1 in the brain tissues in low-dose taurine group were significantly higher than that in high-dose taurine group (P<0.05).The positive staining of GLUT3 only appeared in the periphery of the third ventricle in each group in the cells with buffy membrane or positive cytoplasm.The expression of GLUT3 in the brain tissues in DBI group was significantly higher than that in sham-operated group (P<0.01).The expression of GLUT3 in the brain tissues in low-and high-dose taurine groups was significantly higher than that in DBI group (P<0.01).Compared with low dose taurine group, the expression of GLUT3 in the brain tissues were significantly increased in high-dose taurine group (P<0.01).The pathological damage of cerebral cortex in low-dose taurine group was obviously alleviated.CONCLUSION: Taurine may take part in the neuroprotective mechanisms in DBI by increasing the expression of GLUT1 and GLUT3 at protein level to maintain the energy supply in brain tissues. 相似文献
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AIM: To investigate the effect of early high-protein diet on glucose metabolism in small-for-gestational-age (SGA) rats and the role of adiponectin-AMP-activated protein (AMPK) signaling in this process. METHODS: Forty-eight neonatal male SGA rats were established by maternal food restriction throughout the period of pregnancy. The animals were randomly divided into SGA control group (CS group, 24 rats) and high-protein intervention SGA group (HPS group, 24 rats) when born. Twenty-four normal neonatal male rats were used as normal control group (CN group). The rats in CN group and CS group were breastfed for 3 weeks and their mothers were provided free access to basic diet. After weaning, they were provided free access to basic diet until 12 weeks of age. The rats in HPS group were breastfed for 3 weeks and their mothers were provided free access to high-protein diet. After weaning, they were provided free access to high-protein diet until 4 weeks of age. At the 4th week of age, they were provided free access to basic diet until 12 weeks of age. From 4 to 12 weeks of age, fasting blood glucose and insulin were measured and homeostasis model assessment of insulin resistance index (HOMA-IR) was calculated. The serum adiponectin level and the visceral fat mass (VFM) were detected. The percentage of VFM to body weight (VFM%) was calculated. The visceral fat was paraffin-embedded and the adipocyte area was determined. The expression of AMPKα,phosphorylated AMPKα (p-AMPKα) and glucose transporter 4 (GLUT4) in skeletal muscle was analyzed. At the 12th week of age, the oral glucose tolerance test (OGTT) was performed. RESULTS: At the 4th week of age, no significant difference of HOMA-IR among groups was observed. At the 12th week of age, HOMA-IR in CS group was significantly higher than that in CN group and HPS group. No significant difference of HOMA-IR between CN group and HPS group was found. From 4 to 12 weeks of age, VFM% and adipocyte area of visceral fat in CS group were significantly higher than those in CN group and HPS group. No significant difference of VFM% and adipocyte area of visceral fat between CN group and HPS group was observed. The level of serum adiponectin, and the expression of p-AMPKα and GLUT4 in skeletal muscle were significantly lower in CS group than those in CN group and HPS group. The protein levels of p-AMPKα and GLUT4 were not significantly different between CN group and HPS group. No significant difference in the expression of AMPKα in skeletal muscle among groups was observed. At the 12th week of age, the area under the curve (AUC) of glucose level in OGTT was higher in CS group than that in CN group and HPS group. No significant difference of AUC of glucose level between CN group and HPS group was found. CONCLUSION: Early high protein diet may improve glucose metabolism in SGA rats, partly by avoiding excessive accumulation of visceral fat and possibly by activating adiponectin-AMPK signal pathway to increase GLUT4 expression. 相似文献
9.
AIM: To investigate whether perioxisome proliferator-activated receptor γ (PPARγ) ligand rosiglitazone regulates suppressor of cytokine signaling 1 (SOCS1) and SOCS3 expression as well as pro-inflammatory/anti-inflammatory responses in RAW 264.7 cell-derived foam cells. METHODS: The concentrations of TNF-α, IL-6 and IL-10 in the cultured supernatant of RAW 264.7 cell-derived foam cells were detected by ELISA, and the ratios of TNF-α/IL-10 and IL-6/IL-10 were calculated. RT-PCR and Western blotting were used to analyze the effects of rosiglitazone on the expression of SOCS1 and SOCS3 at mRNA and protein levels. RESULTS: The concentrations of TNF-α, IL-6 and IL-10, and ratios of TNF-α/IL-10 and IL-6/IL-10 in foam cell group were obviously higher than those in control group, but the concentrations of the above factors in oxidized low-density lipoprotein (ox-LDL) +rosiglitazone group were apparently lower than those in foam cell group. The expression of SOCS1 and SOCS3 at mRNA and protein levels in oxLDL+rosiglitazone group was apparently higher than that in control and foam cell group. CONCLUSION: PPARγ ligand rosiglitazone up-regulates the expression of SOCS1 and SOCS3 at mRNA and protein levels and regulates the balance of pro-inflammatory/anti-inflammatory responses in RAW 264.7 cell-derived foam cells. 相似文献
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AIM: To investigate the imbalance between the expression of metalloproteinases (MMPs) and that of tissue inhibitors of metalloproteinase (TIMPs) during wound healing in diabetic rats. METHODS: Diabetic rats were induced with streptozotocin. All rats were maintained for 6 weeks. A full-thickness excisional wound was created on the back of each rat. Every group was randomly divided into 3 subgroups of 7 rats: 3 d group, 7 d group, 14 d group and animals were killed at 3rd, 7th and 14th day. Routine pathological examination, Masson′s trichrome staining and immunohistochemistry were made to calculate the score of epidermal and dermal regeneration, granulation tissue thickness, angiogenesis, matrix density, and infiltrated cells at different time points. RT-PCR and Western blotting were used to detect the expression of mRNA and protein of MMP-9 and TIMP-1 in the skin at those time points. RESULTS: Six weeks after streptozotocin treatment, Three days after injury, the wound healing rate of normal rats was faster than that of diabetic rats. From 3rd to 14th day, there were a lot of fibroblast and macrophage in normal skin, while few such cells were observed in diabetic skin. The other histological scores in normal skin were higher than those in diabetic rats at 7th and 14th day. Both MMP-9 and TIMP-1 had minimally detectable levels before wounding but exhibited rapid, significantly large increases within 3 d after wounding. Subsequently, they showed a rapid decline by 14 d. The relative values of expression of MMP-9 mRNA and protein in diabetic group were higher than those in normal group at different time points. However, the values of TIMP-1 mRNA and protein in diabetic group were significantly lower than those in control group. Significant difference was observed between two groups with the ratio of MMP-9/TIMP-1, higher in diabetic group than that in normal group. CONCLUSION: Abnormal reepithelialization, angiogenesis, inflammatory cell infiltration, collagen fibers generation, granulation tissue deposition, seem to be the basic histopathology that delays wound healing. The imbalance between MMPs and TIMPs in diabetic skin tissue before and after injury may be one of the important reasons of these alterations of histopathology. 相似文献
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AIM: To investigate the potential mechanisms of renoprotective effect of grape seed proanthocyanidin (GSP) on diabetic nephropathy.METHODS: Male Wistar rats were injected with 1% streptozotocin (STZ) intravenously to induce diabetes mellitus (DM). The diabetic rats were randomly divided into 2 groups: diabetes group (DM group) and GSP treatment group (GSP group, GSP 250 mg·kg-1·d-1). The normal Wistar rats served as control (C group). Body weight (BW), systolic pressure, kidney weight/body weight (KW/BW), fasting plasma glucose (FPG), blood urea nitrogen (BUN), serum creatinine (SCr), glycosylated hemoglobin (HbA1c) and 24 h urine protein were determined 24 weeks after STZ intervention. The pathological changes of the renal tissues were observed. The protein levels of glutathione S-transferase mu (GSTM) and nuclear factor-erythroid 2-related factor 2 (Nrf2) in the renal tissues were determined by Western blotting and immunohistochemistry. RESULTS: Compared with C group, BW in diabetic rats decreased (P<0.01). The levels of systolic pressure, FPG, HbA1c, KW/BW, 24 h urine protein, BUN and SCr in DM group were higher than those in C group (P<0.01). After treated with GSP, the levels of systolic pressure, KW/BW, 24 h urine protein, BUN and SCr in DM rats were lower than those in DM rats without treatment (P<0.01 or P<0.05). The pathological changes were ameliorated in GSP group. The expression of GSTM and Nrf2 was up-regulated in the kidneys of diabetic rats and down-regulated to the normal levels after GSP treatment. CONCLUSION: The renoprotective effect of GSP is associated with the down-regulation of GSTM through modulating the expression of Nrf2. 相似文献
14.
WU De-pei XIAO Ying ZHANG Ying-ying ZENG Ling-ping SHI Ming-jun WANG Yuan-yuan GUO Bing 《园艺学报》2016,32(11):2015-2019
ATM:To observe the expression change of PTEN and autophagy in the renal tissues of diabetic rats, and to explore the regulatory mechanism of PTEN/AKT/mTOR pathway to autophagy in diabetic nephropathy. METHODS: The Sprague-Dawley rats were randomly divided into normal control group and diabetic group (8 in each group). The diabetic rat model was established by injection of streptozotocin. The biochemical and kidney indexes were measured after the model of diabetic nephropathy was successfully established. The expression location of PTEN in the renal tubular epithelial cells was observed by the method of immunohistochemistry. The protein levels of autophagy-related protein LC3, PTEN and PTEN/AKT/mTOR signalling molecules were determined by Western blotting. The mRNA expression of PTEN was detected by real-time PCR. RESULTS: The blood glucose, 24 h urine protein and kidney index in diabetic group were all obviously higher than those in control group. Compared with control group, the protein levels of LC3I and LC3II in diabetic group were obviously decreased. PTEN was mainly located in the renal tubular epithelial cells. Compared with control group, the protein expression of PTEN was significantly down-regulated in diabetic group. Furthermore, the activity of PTEN/AKT/mTOR pathway increased in diabetic nephropathy rats. CONCLUSION: The level of autophagy in renal tissues of diabetic rats is decreased, whereas the activity of PTEN/AKT/mTOR pathway is increased. The level of autophagy may be mediated by PTEN/AKT/mTOR pathway. 相似文献
15.
ZHENG Xu-hao ZHANG Xiao-lei JIANG Li-bo HU Xu-qi JIN Yong-long ZHENG Yi-jing WU Wei XU Hua-zi 《园艺学报》2013,29(11):2011-2016
AIM:To explore the levels of apoptosis and autophagy in the nucleus pulposus tissues of intervertebral discs in diabetic rats. METHODS:Sixteen weeks after injection of streptozocin (STZ), the lumbar intervertebral discs were obtained from the rats. The histological changes were observed by hematoxylin-eosin (HE) staining and alcian blue staining. The apoptosis of the nucleus pulposus cells was measured by the methods of terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL), immunohistochemistry, and Western blotting. The level of autophagy in the nucleus pulposus cells was detected by Western blotting and immunohistochemistry. RESULTS:Compared with normal group, HE and alcian blue staining suggested that the intervertebral discs of the diabetic rats became degenerate. The expression of caspase-3 and the apoptotic rate were increased in intervertebral disc nucleus pulposus of the diabetic rats. The results of immunohistochemistry and Western blotting showed that the expression levels of LC3Ⅱ/LC3Ⅰand beclin-1 in the diabetic rats were higher than those in normal group. CONCLUSION: The STZ-induced diabetes accelerates degeneration of the intervertebral discs. In addition, the apoptosis and autophagy are increased in the intervertebral discs of diabetic rats. 相似文献
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ATM: To investigate the effect of oxymatrine (OXY) on high fat-induced insulin resistance in mice, and to investigate the mechanism. METHODS: ApoE-/-mice with high-fat diet for 16 weeks were divided into insulin resistance group, and OXY groups at concentrations of 25, 50 and 100 mg/kg. C57BL/6J mice served as normal control group. The mice in OXY groups were gavaged with OXY for 8 weeks. Glucose tolerance test in the mice was performed. Fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG), fatty acid (FFA) and fasting insulin (FINS) in the plasma were measured. The mRNA expression of insulin receptor (INSR), insulin receptor substrate-2 (IRS-2), glucose transporter 2 (GLUT2) in the liver tissues was examined by RT-qPCR. The protein levels of GLUT2, INSR, IRS-2, p-INSR, p-IRS-2, PI3K, p-PI3K, serine/threonine protein kinase (AKT) and p-AKT were examined by Western blot.RESULTS: OXY reduced the levels of FBG, TC, TG, FFA and FINS, and attenuated insulin resistance. Compared with insulin resistance group, the mRNA expression of INSR, IRS-2 and GLUT2 significantly increased in OXY groups (P<0.05). The protein levels of p-INSR/INSR, p-IRS-2/IRS-2, p-PI3K/PI3K, p-AKT/AKT and GLUT2 also increased in OXY groups (P<0.05).CONCLUSION: OXY ameliorates high fat-induced insulin resistance in mice via PI3K/AKT pathway. 相似文献
17.
WANG Jing-ru ZHAO Jing-jing YE Chun-ling YE Kai-he ZHANG Xiao-qi WANG Ying YE Wen-cai 《园艺学报》2012,28(6):1109-1113
AIM: To investigate the effects of total triterpenoids from Psidium guajava leaves (TTPGL) on blood glucose and lipids in type 2 diabetic rats. METHODS: The diabetic rats were induced by intraperitoneal injection of streptozotocin at dose of 35 mg/kg and feeding with high-fat diet. The animals were divided into 5 groups: diabetic model control group (model), TTPGL treatment groups (with the doses of 60, 120 and 240 mg/kg, respectively) and rosiglitazone treatment group (3 mg/kg). Another 12 normal SD rats were used as the normal controls. The rats received daily treatment for 6 weeks, and then the levels of fasting blood glucose (FBG), fasting insulin (FINS), triglyceride (TG), total cholesterol (TCH), free fatty acid (FFA), glycosylated hemoglobin (GHb) and glycosylated serum proteins (GSP) were measured. The protein expression of peroxisome proliferator-activated receptor γ (PPARγ) in adipose tissues was detected by Western blotting. RESULTS: Compared with normal control group, the levels of FBG, GHb and blood lipids were increased in type 2 diabetic rats. The FINS, insulin sensitivity index, and the protein expression of PPARγ in adipose tissues were decreased. Compared with model group, the levels of FBG and GSP were decreased,and the FINS, insulin sensitivity index, and the protein expression of PPARγ in adipose tissues significantly increased in TTPGL treatment groups (with the doses of 120 and 240 mg/kg). The levels of serum TG,TCH and FFA were significantly lower in TTPGL treatment groups (P<0.01 or P<0.05) as compared with the model controls. CONCLUSION: TTPGL decreases the levels of blood glucose and lipids in diabetic rats. TTPGL also increases serum insulin level and improves insulin sensitivity. The action mechanism of TTPGL may be related to the increase in the protein expression of PPARγ. 相似文献
18.
AIM: To study the effect of high fat diet on the expression of sterol regulatory element biding protein-1 (SREBP-1) and transforming growth factor β1 (TGF-β1) in renal tubular cells and rosiglitazone intervention. METHODS: Wistar rats were treated with high fat diet and rosiglitazone for 3 months. The serum glucose, serum insulin and serum triglyceride were detected. Oil Red O staining was used to observe the renal lipid deposit and Masson staining was for the detection of ECM accumulation. SREBP-1, TGF-β1 and FN protein were determined by the methods of immunohistochemistry and Western blotting. SREBP-1 mRNA was detected by in situ hybridization. RESULTS: Rosiglitazone prevented effectively the increase in serum glucose, serum insulin and serum triglyceride resulted from high fat diet. High fat diet led to lipid droplet formation in renal tubular cells and interstitial ECM accumulation, which was decreased by rosiglitazone treatment. Compared to normal rats, SREBP-1 protein and SREBP-1 mRNA showed high expressions in high fat diet rats that were lowered by rosiglitazone. The precursor segment and mature segment of SREBP-1 protein were decreased by 27.39% and 27.32%. Similarly, the high expressions of TGF-β1 and FN protein in kidney of high fat diet rats were also prevented by rosiglitazone intervention. Compared to high fat diet rats, the expression of TGF-β1 in rosiglitazone treatment rats was lowered by 19.14%. CONCLUSION: Rosiglitazone prevents effectively the over-expression of SREBP-1 and TGF-β1 in renal tubular cells, and decreases lipid accumulation and ECM production in rats fed with high fat diet. 相似文献
19.
WANG Ling XU Meng-fei LIU Xi WANG Wei-wei CHEN San-mei CHENG Jin-guo CHEN Guo-rong 《园艺学报》2014,30(2):328-338
AIM:To observe the protective effect of curcumin derivative B06 on the liver from the rats with hyperlipidemia and type 2 diabetes mellitus. METHODS:Male Sprague-Dawley rats (n=35) were divided randomly into 5 groups: normal control group, high-fat group, high-fat+B06-treated group, diabetic group and diabetic +B06-treated group. After fed with a high-fat diet for 4 weeks, the rats in the later 2 groups were injected with streptozotocin intraperitoneally to induce type 2 diabetes mellitus. The rats in B06-treated groups were given B06 by gavage at a dose of 0.2 mg· kg-1·d-1 for 8 weeks. After the treatment, the morphology of the liver was observed under light and transmission electron microscopes. The protein expression of AMP-activated protein kinase α (AMPKα) and phosphorylated AMPK α (p-AMPKα) was detected by Western blotting. RESULTS:Fatty degeneration, hepatocellular necrosis, inflammatory cell infiltration and hyperplasia of fibrous tissue were observed in the liver from the rats in high-fat group and diabetic group,and were relieved after B06 treatment. The protein expression of p-AMPKα was decreased in the liver of the rats in diabetic group and high-fat group, and it was increased in the liver of the high-fat and diabetic rats in B06-treated group. CONCLUSION:Curcumin derivative B06 exerts a protective effect on the liver in type 2 diabetic rats, and the increased expression of p-AMPKα may be involved in the mechanism of protection. 相似文献
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HAO Jun WANG Chen WU Hai-jiang ZHAO Song DUAN Jian-zhao SHI Yong-hong DUAN Hui-jun 《园艺学报》2009,25(3):566-571
AIM:To investigate the expression of sterol regulatory element binding protein-1 (SREBP-1) and sterol regulatory element binding protein-2 (SREBP-2) in the kidney of type 1 diabetic rats.METHODS:The triglyceride (TG) and cholesterol content in the kidney of experimental rats were measured by the assay kits and oil red O staining.Furthermore, the expressions of SREBP-1 and SREBP-2 protein were detected by the methods of Western blotting and immunohistochemistry.The analysis of SREBP-1 mRNA was performed by in situ hybridization.RESULTS:Renal triglyceride content was markedly higher in diabetic rats than that in normal rats and the result of oil red O showed that lipid deposited in the renal tubular epithelium.Immunohistochemistry and Western blotting presented similar results that SREBP-1 protein was up-regulated in renal tubular epithelium in diabetic rats.On the other hand, SREBP-2 protein didnt show difference between diabetic rats and normal control rats.In situ hybridization confirmed the increasing of SREBP-1 mRNA in renal tubular epithelium in diabetic rats.CONCLUSION:Above results suggest that altered SREBP-1 may play an important role in the pathogenesis of renal lipid accumulation in type 1 diabetic rats. 相似文献