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1.
AIM: To explore the role of DNA methylation of microRNA-30a-5p(miR-30a-5p) promoter region in hepatic injury. METHODS: Four-week-old normal mice and cystathionine β-synthase (CBS) single gene knockout mice were used and divided into normal (CBS+/+, n=12) group and single gene knockout (CBS+/-, n=12) group, and the mice were fed with high methionine diet for 8 weeks. HL-7702 hepatic cells were routinely cultured in vitro and divided into control group, homocysteine (Hcy) group and Hcy+5-azacytidne (AZC) group. Serum Hcy, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured by automatic biochemical analyzer. The levels of ALT and AST in the cells culture medium were determined by the microplate method. Hepatic injury in the mice were observed with HE staining. Cell viability staining was used to measure the viability of hepatocytes. RT-qPCR was used to detect the expression of miR-30a-5p in the liver tissues and hepatocytes. The correlation between the expression of miR-30a-5p and serum ALT and AST levels was analyzed by Pearson correlation analysis. DNA methylation level of miR-30a-5p promoter region in the liver tissues and hepatocytes was detected by nested landing methylation-specific PCR (nMS-PCR). RESULTS: Compared with the CBS+/+ mice, the serum levels of Hcy, ALT and AST in the CBS+/- mice were significantly increased (P < 0.05). HE staining showed the hepatocyte swelling and nuclear fragmentation and dissolution. The expression level of miR-30a-5p in the liver tissues was decreased (P < 0.01). Besides, the expression level of miR-30a-5p in the mice was negatively correlated with serum ALT and AST levels (r2=0.4557, P=0.0003, r2=0.4626, P=0.0003), and the DNA methylation of miR-30a-5p promoter region was increased (P < 0.01). In the HL-7702 cells, compared with control group,the ALT and AST levels were increased in Hcy group (P < 0.05, P < 0.01), and the cell viability was remarkablely decreased. DNA methylation of miR-30a-5p promoter region was increased (P < 0.01), which decreased after treated the cells with AZC (P < 0.05), while the expression level of miR-30a-5p in the cells was increased (P < 0.05). CONCLUSION: Hypermethylation of miR-30a-5p promoter region may play an important role in hepatic injury.  相似文献   

2.
AIM:To study the effect of adoptive transfer of CD4+ T cells with microRNA-7 (miR-7) knockdown (KD) on mouse acute liver injury model and to investigate its significance. METHODS:CD4+ CD62L+ T cells were purified from the spleen of normal wild-type (WT) mice and miR-7KD mice by magnetic bead sorting, and were stained with CFSE. These 2×106 CFSE-labeling cells were injected into normal mice via tail vein, and then the mouse acute liver injury model was induced by intraperitoneal injection of 30 mg/kg concanavalin A. After 72 h, the appearance, weight and weight index of the liver were investigated. The pathological change of the liver tissues was observed by HE staining. Real-time PCR was used to examine the mRNA expression of Bax and P53. The expression levels of CD62L, interleukin-4 (IL-4) and interferon-γ (IFN-γ) in the CD4+ T cells were analyzed by flow cytometry. RESULTS:We found that the liver tissue became lighter, and the weight (P<0.01) and weight index (P<0.05) were changed significantly in miR-7KD mice compared with control group. Moreover, HE staining showed that the liver cell damage was increased in the liver of miR-7KD mice. Meanwhile, the expression levels of Bax and P53 were significantly increased in miR-7KD group (P<0.05). The percentage of CD62L in CD4+ T cells was significantly decreased (P<0.01) in miR-7KD mice, with high expression of IFN-γ (P<0.05) and low expression of IL-4 (P<0.01) in CD4+T cells. CONCLUSION:These findings suggest that miR-7 knockdown significantly promotes the pathology of CD4+ T cell-mediated acute liver injury, which provides a preliminary experimental basis for further exploration on the mechanism of acute liver injury occurrence.  相似文献   

3.
AIM: To study the effect of microRNA-7 (miR-7) knockdown (KD) on concanavalin A (ConA)-induced acute liver injury (ALI) in mice.METHODS: Wild type (WT) mice and miR-7KD mice were received ConA (30 mg/kg) to induced acute liver injury model by intraperitoneal injection, and the morphological changes, liver weight and weight index were measured 48 h later. The pathological changes of the liver tissues were observed by HE staining. The levels of serum alanine aminotransferase (ALT), IL-4 and IFN-γ were detected by ELISA. The proportional changes of CD4+ T cells and the relative levels of IL-4 and IFN-γ were analyzed by flow cytometry.RESULTS: The color of the liver tissue became lighter, and the weight and weight index were changed significantly in miR-7KD mice compared with control group (P<0.05). HE staining showed that the inflammatory cell infiltration was increased in the liver of miR-7KD mice. Moreover, the level of serum ALT was significantly increased (P<0.05). The serum level of IFN-γ elevated significantly (P<0.01), while the IL-4 levels decreased significantly (P<0.01) in the serum of miR-7KD mice. Furthermore, the proportion of CD4+ T cells and relative IFN-γ cells increased obviously (P<0.01).CONCLUSION: miR-7 knockdown promotes the pathogenesis of the ConA-induced acute liver injury in mice.  相似文献   

4.
AIM: To investigate the effects of antioxidant N-acetylcysteine (NAC) on the lipopolysaccharide (LPS)-induced MAPK phosphorylation in mouse liver. METHODS: 54 male mice were divided into three groups: control (n=6), 0.9% sodium chloride 0.2 mL ip; LPS group (n=24): LPS 5 mg ip; NAC+LPS group (n=24): NAC 150 mg·kg-1·d-1 ip, for 3 d; LPS 5 mg ip after 1 h of NAC administration at 3rd day. The liver was excised with carbrital anesthesia after LPS or 0.9 % sodium chloride injection at 0.5 h, 1 h, 2 h and 6 h for GSH and MDA assays. The protein extracted from liver was assayed for the phosphorylation of MEK1/2, ERK1/2, p38 MAPK by Western blotting. TNF-α in liver was assayed by radioimmunoassay. RESULTS: MDA in the liver was decreased remarkably and the GSH in the liver was increased significantly by NAC pretreatment. The phosphorylation of MEK1/2, ERK1/2 and p38 MAPK in liver were inhibited significantly by NAC pretreatment after LPS challenge. Meanwhile, TNF-α in liver was decreased markedly. CONCLUSION: Reactive oxygen species plays a critical role in MAPK signaling during the LPS induced acute liver injury. NAC partially inhibits LPS-induced MAPK signaling by antioxidant effect and decreases TNF-α production.  相似文献   

5.
AIM: To investigate the effects of dexmedetomidine (DEX) on acute alcoholic hepatic injury in mice and to explore the possible mechanisms. METHODS: Kunming mice (n=50) were randomly divided into 5 groups (n=10): normal saline control (NS) group, acute alcoholic hepatic injury model (E) group, low-dose (10 μg/kg) DEX (E+L) group, medium-dose (50 μg/kg) DEX (E+M) group and high-dose (100 μg/kg) DEX (E+H) group. The animals were sacrificed at 6 h after gavage of alcohol or normal saline. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) were measured. The livers were removed for evaluation of histological characteristics and determining the content of tumor necrosis factor-α (TNF-α) amd interleukin-1β (IL-1β) in the liver tissues by ELISA. The expression levels of cytochrome P450 2E1 (CYP2E1) and nuclear factor-κB (NF-κB) in the liver tissues were evaluated by Western blot. RESULTS: Compared with NS group, the levels of ALT, AST and TG were obviously increased in E group, which were obviously decreased in E+M and E+H groups. Compared with NS group, the levels of TNF-α, IL-1β and MDA were obviously increase in E group, which were obviously decreased in E+M and E+H groups. Compared with NS group, the activity of SOD and the content of GSH were obviously decreased in E group, which were obviously increased in E+M and E+H groups. Compared with NS group, the expression of CYP2E1 and NF-κB was obviously increase in E group, which was obviously decreased in E+M and E+H groups. Compared with NS group, ethanol induced marked liver histological injury, which was less pronounced in E+M and E+H groups. CONCLUSION: DEX has a protective effect on mouse liver with acute alcoholic injury by the involvement in the processes of antioxidation and antiinflammation, and its mechanism may be associated with the inhibition of CYP2E1 and NF-κB expression.  相似文献   

6.
AIM: To investigate the effect of microRNA-17 (miR-17) on the senescence of vascular smooth muscle cells (VSMCs) and the underlying mechanism.METHODS: The medial layer of the thoracic aorta was collected from the SD rats and isolated for primary culture. VSMCs were identified by immunofluorescence staining. The VSMCs were collected at the 4th~6th generations, and then the miR-17 mimics and miR-17 inhibitor were transfected into the VSMCs by liposome method. After 24 h, the cell senescence was induced by D-galactose. The VSMCs were divided into the following 6 groups:aging induction+miR-17 mimics (A-miR-17) group, aging induction+miR-17 inhibitor (A-anti-miR-17) group, A-control group, normal (N)+miR-17-mimics (N-miR-17) group, N-anti-miR-17 group, and N-control group. On day 3 after the addition of D-galactose, the senescence of VSMCs was observed with β-galactosidase staining. The expression of miR-17, p16 and p21 was detected by RT-qPCR and immunohistochemistry. RESULTS: miR-17 expression in the VSMCs was significantly lower in A-control group than that in N-control group (P<0.01). Compared with A-control group, the expression of miR-17 in the VSMCs was significantly increased in A-miR-17 group (P<0.01), while that was significantly decreased in A-anti-miR-17 group (P<0.01). The number of β-galactosidase positive staining cells in A-anti-miR-17 group was significantly higher than that in A-miR-17 group (P<0.01). The expression of p21 at mRNA and protein levels in the VSMCs was significantly lower in A-miR-17 group than that in A-control group (P<0.01), and the expressions of p21 at mRNA and protein levels was significantly higher in A-anti-miR-17 group than that in A-miR-17 group (P<0.01). CONCLUSION: miR-17 inhibits rat VSMCs senescence induced by D-galactose, the underlying mechanism is associated with the inhibition of p21 expression.  相似文献   

7.
AIM: To investigate the effect of cepharanthine on the growth of human lung carcinoma A549 cells and the underlying mechanism. METHODS: After A549 cells were treated with cepharanthine, the growth inhibitory rate was detected by MTT assay. The cell morphological changes were observed under light microscope. The apoptosis of the A549 cells was analyzed by flow cytometry. The expression of microRNA (miR)-150, miR-182, p53 mRNA and FOXO1 mRNA were detected by real-time PCR. The downstream target genes were predicted by software, and the expression of p53 and FOXO1 was determined by Western blot. RESULTS: After cepharanthine treatment, the growth of A549 cells was inhibited, the apoptosis rate was significantly increased, and the expression levels of miR-150 and miR-182 were significantly decreased. With cepharanthine treatment at 10 μmol/L, the expression levels of p53 and FOXO1 were elevated; however, with cepharanthine at 30 μmol/L, the expression levels of p53 and FOXO1 were decreased. After transfection with miR-150, the expression of p53 was significantly decreased, while the expression of FOXO1 was significantly decreased after transfection with miR-182. CONCLUSION: Cepharanthine inhibits the growth of A549 cells and promotes the apoptosis of A549 cells by inhibiting the expression of miR-150 and miR-182. miR-150 and miR-182 may down-regulate the expression of p53 and FOXO1, respectively.  相似文献   

8.
AIM: To examine the role of glucocorticoid receptor (GR) in regulation of lipopolysaccharide (LPS)-induced lung injury. METHODS:Male Sprague-Dawley rats were divided into six groups randomly: control group (n=6), LPS group (n=6 each), Dex+LPS group (n=6 each), RU486 group (n=6), RU486+LPS group (n=6 each) and RU486+Dex+LPS group (n=6 each). All groups were subjected into 1 h, 3 h, 6 h and 12 h time point subgroups after LPS administration, except of control group and RU486 group. The concentrations of TNF-α and IL-6 in bronchoalveolar lavage fluids (BALF) were detected by ELISA. The histopathologic changes of lung tissues, the activation of p38MAPK and the expression of MKP-1 in lung tissue were also observed. Further, to confirm the role of GR in this model, the mortality of rats in LPS group vs RU486+LPS group and in Dex+LPS group vs RU486+Des+LPS group was compared. RESULTS: LPS induced lung injury and the secretions of TNF-α and IL-6 in BALF, which were significantly enhanced by pretreatment of RU486 (P<0.05). RU486 pretreatment also significantly increased the LPS-induced lethality (P<0.05). Dexamethasone attenuated LPS-induced lung damage, cytokine release and mortality rates, and the protective effects might be mediated by GR. Western blotting analysis showed dexamethasone inhibited the phosphorylation of p38MAPK in lung tissues by induction of MKP-1, and these actions were also GR dependent. CONCLUSION: GR plays an essential role in regulation of LPS-induced acute lung injury. Anti-inflammatory effects of hormone-activated GR may be mediated by inhibition of p38MAPK phosphorylation/activation, which is associated with the induction of MKP-1.  相似文献   

9.
AIM: To investigate the effect of microRNA-214-5p (miR-214-5p) on myocardial injury and immune response in rats with ischemia-reperfusion (I/R) by targeting p21-activated protein kinase 4 (PAK4). METHODS: The rats were divided into sham group, I/R group, Ad-Scramble group, and Ad-miR-214 group (n=9). Adenovirus was injected into 6 different sites on the anterior wall of the left ventricle of the rats. Four days later, the I/R model was constructed by suturing the left anterior descending coronary artery. The expression level of miR-214 was detected by RT-qPCR. Myocardial injury was observed by HE staining. The levels of heart damage markers (CK-MB, Mb, and cTnI) and inflammatory factors (IL-6, IL-1β and TNF-α) were measured by ELISA. The rate of cardiomyocyte apoptosis was analyzed by flow cytometry. The content of MDA and the activity of SOD were detected by commercially available kits. Target genes were predicted by genetic software and verified by dual-luciferase reporter assay. The protein levels of caspase-3, caspase-9, Bcl-2, Bax, PAK4, p-Akt and p-mTOR were determined by Western blot. RESULTS: miR-214 was down-regulated in the cardiomyocytes of I/R rats (P<0.01). Over-expression of miR-214-5p attenuated myocardial injury in the I/R rats, down-regulated the expression of CK-MB, Mb and cTnI, decreased the apoptotic rate of cardiomyocytes, up-regulated the expression of Bcl-2, down-regulated Bax, caspase-3 and caspase-9 expression, increased SOD activity, and decreased the content of MDA, IL-6, IL-1β and TNF-α (P<0.01). The binding sites of miR-214-5p and PAK4 were pre-sent in the 3’-UTR, and over-expression of miR-214-5p up-regulated the protein levels of PAK4, p-Akt and p-mTOR (P<0.01). CONCLUSION: miR-214-5p over-expression attenuates myocardial injury in I/R rats by targeting PAK4, inhibits cardiomyocyte apoptosis, oxidative stress and inflammation, and activates the PI3K/Akt/mTOR pathway.  相似文献   

10.
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11.
AIM: To investigate the effect of scutellarin on resuscitating rat non-heart-beating marginal donor (NHBMD) livers with extracorporeal liver perfusion in vitro. METHODS: Twenty-four male Wistar rats were randomly divided into 3 groups: group A (n=8), the livers were subject to 15~20 min of warm ischemia; group B (n=8) and group C (n=8), the livers were subject to 45 min of warm ischemia. All the livers were treated by extracorporeal liver perfusion (ECLP), and scutellarin solution was add to the perfusion fluid in group C with the intervals of 1 h. The data of bile production and the markers of hepatocyte reperfusion injury of the livers,alanine aminotransferase (ALT) and endothelin-1 (ET-1), in each group were tested. The liver tissues in each group were obtained before perfusion and 1 h, 3 h and 6 h after perfusion, and then observed under transmission electron microscope to investigate the changes of ultrastructures. RESULTS: With the time of perfusion went on, the livers in group B and group C demonstrated recovery of synthe-tic function after 3 h and 6 h of perfusion, and the production of bile in group B and group C was not significantly different from that in group A after 6 h of perfusion (P>0.05). The levels of ALT and ET-1 in group B and group C were significantly higher than those in group A after 1 h, 3 h and 6 h of perfusion (P<0.05), and those in group C was significantly lower than those in group B after 3 h and 6 h of perfusion (P<0.05). The ultrastructural destruction of the liver cells in both group B and group C was more serious than that in group A. After 3 h and 6 h of perfusion, the destruction of the liver cells was partly recovered, and the recovery degree in group C was more obvious than that in group B. CONCLUSION: Scutellarin may play a significant role in resuscitating rat NHBMD livers with extracorporeal liver perfusion in vitro.  相似文献   

12.
AIM: To investigate the molecular mechanism of microRNA-21 (miR-21) in the regulation of Schwann cell proliferation following nerve injury. METHODS: The expression of miR-2l was detected by real-time PCR. Synthetic miR-21 mimic and its control were transfected into rat Schwann cells. CCK-8 assay was performed to evaluate the influence of miR-21 on the proliferation of Schwann cells. The cell cycle distribution was determined by flow cytometry. The expression of transforming growth factor β-induced protein (TGFBI) and cyclin D1 were detected by Western blotting. RESULTS: The expression of miR-21 in model group was 7.87±0.75 and 7.75±0.80 times higher than that in sham operation group and blank group respectively. After transfected with miR-21 mimic, the expression of miR-21 in experimental group was 2.21±0.14 and 2.29±0.21 times higher than that in negative control group and blank group respectively. Moreover, the A450 value of CCK-8 assay in experimental group at 48 h was higher than that in negative control group and blank group. The proliferation index in experimental group was higher than that in negative control group and blank group. At the same time, the expression of TGFBI obviously decreased and the cyclin D1 increased in the Schwann cells 48 h after transfection with miR-21. CONCLUSION: miR-21 promotes the proliferation activity of Schwann cells by down-regulating TGFBI expression.  相似文献   

13.
AIM: To explore the relationship and molecular mechanism between microRNA-21(miR-21) and Schwann cells (SC) following peripheral nerve injury. METHODS: The mRNA expression of miR-21 and phosphatase and tensin homologue deleted on chromosome ten (PTEN) in animal model were detected by real-time PCR. The over-expression of miR-21 and inhibition of miR-21 expression in the Schwann cells according to transfection of lentiviral vectors were performed, the nonspecific miRNA was used as a negative control (NC). The cell apoptosis was measured by flow cytometry. The mRNA expression of miR-21 and PTEN in the cells was detected by real-time PCR. The protein expression of PTEN and cleaved caspase-3 was determined by Western blot. RESULTS: The level of miR-21 was significantly higher and the mRNA level of PTEN was significantly lower in the model of nerve injury than those in control group. miR-21 over-expression decreased the number of apoptotic Schwann cells compared with NC-SC. The mRNA expression of PTEN was down-regulated by over-expression of miR-21. The protein expression of PTEN and cleaved caspase-3 was down-regulated by over-expression of miR-21(P<0.05). CONCLUSION: miR-21 may play an important role in the peripheral nerve injury through inhibiting apoptosis of Schwann cells by down-regulating the expression of PTEN.  相似文献   

14.
AIM: To observe the expression of apoptosis regulating proteins Bcl-2, Bax and the changes of cortical somatosensory evoked potential (CSEP), motion evoked potential (MEP) after acute spinal cord injury, and to explore the relationship between them. METHODS: Fifty six Wistar rats were randomly divided into 7 groups. Six groups were divided as acute spinal cord injury model, the other group was used as control. CSEP and MEP were monitored after 0 h, 6 h, 12 h, 24 h, 48 h and 72 h. The spinal cord was taken and then HE staining and immunohistochemistry methods were used to study the pathology changes and expressions of Bcl-2 and Bax. RESULTS: The peak of CSEP and MEP showed a immediate drop or disappear, and then partially raised at 6 h, declined again at 12 h and partially raised at 24 h, and then raised obviously at 48 h, the peak still lower than normal at 72 h. Changes of the peak value showed a double posture of decreased-raised- declined again and raised again. The incubation period of peaks extended corresponding to the different degrees. There was a weak positive expression of Bcl-2 and Bax at 6 h after injury. By 24 h after injury, the positive expression of Bcl-2 was maximal and the positive expression of Bax was maximal at 12 h after injury. CONCLUSION: The changes of CSEP and MEP have a very closely correlation to the degree of spinal cord injury. CSEP and MEP may serve as electrophysiological indicators to judge the motor function and the prognosis after acute spinal cord injury.  相似文献   

15.
AIM: To investigate the expression pattern of apolipoprotein M (apoM) protein in renal cortex of acute renal failure (ARF) rats with reperfusion. METHODS: Seventy-five male rats were randomly divided into sham operation group (n=25), ARF group (n=25) and pyrrolidine dithiocarbamat (PDTC) group (n=25), five subgroups at time points of 3 h, 6 h, 12 h, 24 h and 48 h after reperfusion were set up in each group. The expressions of apoM in cytoplasm and NF-κB p65 in nucleus of renal cortex were detected at the indicated time points. RESULTS: The expression of apoM in ARF group was obviously higher than that in sham operation group (P<0.01), and two peaks were detected, the first peak was at 6 h after reperfusion, while the second one was from 24 h to 48 h. The tendency of apoM expression in PDTC group was similar to that in ARF group, while the expression in every subgroup was prevalently lower than that in ARF group (P<0.01). Otherwise, a significant correlation (r=0.852, P<0.01) was found between the expression of apoM and NF- κB p65. CONCLUSION: The results indicate that apoM feasibly take part in the pathogenesis of ARF through the inflammatory reaction mediated by NF-κB.  相似文献   

16.
AIM: To explore the effects of Auricularia (A.) auricula-judae extracts on the liver function in septic rats. METHODS: Forty male Wistar rats were randomly divided into control group, model group, A. auricula-judae polysaccharide group and A. auricula-judae crude extract group. Septic model was induced by the procedure of cecal ligation and puncture (CLP). Intragastric administration was performed every 8 h 3 days prior to CLP. The plasma levels of alanine aminotransferase(ALT), aspartate aminotransferase(AST), endotoxin(ET), tumor necrosis factor α(TNF-α), interleukin 6(IL-6) and IL-1β were detected 12 h after CLP. The specimens of the liver were collected to observe the pathological changes. The expression of NF-κB in the liver tissues was detected by the method of immunohistochemistry. RESULTS: Compared with the CLP rats, the intervention of A. auricula-judae polysaccharide and A. auricula-judae crude extract to the septic rats significantly decreased the serum levels of ALT, AST, ET, TNF-α, IL-1β and IL-6 (P<005). The pathological changes of the liver tissues in treatment groups were significantly attenuated compared with CLP group. CONCLUSION: A. auricula-judae polysaccharide and A. auricula-judae crude extract protect liver against sepsis-induced injury by inhibiting the systemic inflammatory response.  相似文献   

17.
AIM: To investigate the protective effects of human acidic fibroblast growth factor (aFGF) on hypothermic preservation of rat liver. METHODS: Twenty-four Wistar rats were randomly divided into 2 groups (n=6): hypertonic citrate adenine (HCA) solution control group and experimental group (aFGF compound solution, containing 40 μg/L aFG14-154 in HCA solution). The isolated livers were preserved in corresponding solution for 12 h or 24 h, and the content of malondialdehyde (MDA), the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and the changes of liver weight in the 2 groups were analyzed. The histopathological changes of the livers were also examined. RESULTS: Compared with HCA control group, the levels of ALT, AST and MDA and the changes of liver weight were significantly decreased in experimental group (24 h), and the changes of liver histopathology were obviously alleviated in experiment group. CONCLUSION: aFGF can reduce rat hepatic injury. The protective effects of aFGF may be related to attenuating cell swelling and improving the capacity of anti-oxidative damage in the liver.  相似文献   

18.
AIM: To explore whether miR-21 low expression enhances the effect of matrine (MAT) on the apoptosis of hepatocellular carcinoma cells.METHODS: Real-time fluorescence quantitative PCR (RT-qPCR) was used to detect the expression of miR-21 in the HepG2 cells treated with different concentrations of MAT. The effect of miR-21 on MAT-induced HepG2 cell apoptosis was analyzed by flow cytometry. The mRNA and protein expression of Bcl-2 and Bax in the HepG2 cells treated with MAT was determined by RT-qPCR and Western blot.RESULTS: The expression of miR-21 increased with the increasing concentration of MAT. Low expression of miR-21 promoted MAT-induced apoptosis, and enhanced the expression of Bax at mRNA and protein levels (P<0.05), while inhibited the expression of Bcl-2 at mRNA and protein levels (P<0.05).CONCLUSION: Low expression of miR-21 enhances MAT-induced HepG2 cell apoptosis by inhibiting the expression of Bcl-2 and promoting Bax expression.  相似文献   

19.
AIM：To explore the effect of intervention for mast cell function before reperfusion on intestinal ischemia-reperfusion (IR)-induced early liver injury. METHODS：Adult SD rats (n=35) were randomized into 5 groups with 7 rats each: sham operation group (S group), IR group, cromolyn sodium treatment group (IR+C group, 25 mg/kg), ketotifen treatment group (IR+K group, 1 mg/kg), compound 48/80 treatment group (IR+CP group, 0.75 mg/kg). IR was induced by superior mesenteric artery occlusion for 75 min followed by 4 h of reperfusion. The agents were intravenously administered 5 min before reperfusion. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and histamine, and the liver levels of lactate dehydrogenase (LDH), tumor necrosis factor α (TNF-α), interleukin-8 (IL-8), malondialdehyde (MDA) and superoxide dismutase (SOD) were assessed. The liver histopathologic changes were also evaluated. RESULTS：IR resulted in severe liver injury as demonstrated by great increases in injury scores, concomitant significant increases in serum levels of AST, ALT and histamine, and liver levels of LDH, TNF-α, IL-8, and MDA, accompanied by reduced SOD activity (all P<0.05 vs S group). Treatment with cromolyn sodium or ketotifen markedly alleviated IR-mediated liver injury as confirmed by significant reduction of the above biomedical changes, whereas compound 48/80 further aggravated liver injury by dramatically enhancing the biomedical changes (all P<0.05 vs IR group). CONCLUSION：Inhibition of mast cell function before reperfusion may reduce early liver injury induced by intestinal ischemia reperfusion. Histamine, oxidative stress and inflammatory response may provide promising effects on it.  相似文献   

20.
AIM:To explore the role of imbalance of local renin-angiotensin system (RAS) in lung injury by observing the changes of angiotensin Ⅱ type 1 receptor (AT1R) and Mas receptor protein expression in the lung and the degree of lung injury subject to limb ischemia-reperfusion (LIR) in the mice.METHODS:Male ICR mice (n=42,8 weeks old) were randomly assigned into 7 groups (6 in each group),including control group and 6 model groups with LIR of 0.5 h,1 h,2 h,4 h,6 h and 12 h reperfusion.Tourniquets were used to block the blood flow of the hind limbs of the ICR mice and were released after 2 h ischemia to initiate reperfusion.The mice were sacrificed by eyeball blood withdrawal at different time points after reperfusion.The organ coefficient and wet/dry weight ratio (W/D) of the lung tissue were calculated.Bronchoalveolar lavage fluid (BALF) was taken for cell counting and protein concentration measurement.The histopathological changes of the lung tissues was observed,and the pathological score was calculated.The protein expression of AT1R and Mas receptor in the lung tissues was determined by Western blot.RESULTS:The organ coefficient,W/D of lung tissue,and cell number and protein concentration in BALF of model groups were significantly higher than those in control group after LIR.The pathological changes were found in the lung tissue of model mice,including alveolar capillary dilation and congestion,edema,inflammatory cell infiltration in peripheral vascular,alveolar and bronchial walls,alveolar septal thickening and inflammatory cell infiltration.The lung injury score was elevated gradually along with the extension of reperfusion time.The protein expression of AT1R began to increase at reperfusion time points of 0.5 h and 1 h.With the extension of reperfusion time,the protein expression of AT1R decreased gradually.Conversely,the protein expression of Mas receptor increased gradually with prolonged reperfusion.CONCLUSION:LIR induces acute lung injury gradually.The imbalance of AT1R and Mas receptor expression may be involved in the damage process.  相似文献   

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