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Epigallocatechin-3-Gallate-Induced Protection And The Underlying Mechanisms On Liver Ischemia-Reperfusion Injury

Posted on:2016-09-11Degree:MasterType:Thesis
Country:ChinaCandidate:X H ZengFull Text:PDF
GTID:2284330461470600Subject:Oncology
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Objective:To investigate of Epigallocatechin-3-gallate (EGCG) on liver ischemia-reperfusion injury and the molecular mechanisms underlying the effect in vivo.Methods:Eighteen male Balb/c mice were randomly divided into three groups(n=6):sham-operated group, ischemia-reperfusion group(I/R group) and EGCG group. The mice were sacrificed at the end of reperfusion, and serum levels of alanine aminotransferase(ALT), aspartate aminotransferase(AST) were measured. HE staining was used to observe the changes of the hepatic histopathological, and Immunohistochemistry was applyed to examine the expression of HO-1, NF-κB P65 and TLR4 protein.Western blotting was employed to examine NF-κB P65 and TLR4 protein expression, and mRNA of HO-1, TLR4, TNF-a, IL-6 and IL-1 was conducted by Real-time PCR.Results:After the pre-treatment with 80mg/kg EGCG, compared with Sham group, I/R group showed significantly increased the serum levels of AST [(1143.33±268.66) vs (349.00±39.24), P<0.01], and ALT [(1295.00±214.39) vs (205.00±28.35), P<0.01], the mRNA levels of TLR4, HO-1, TNF-α, IL-6 and IL-1β, the protein level of TLR4, HO-1 and NF-κB P65 in left lobe of liver tissue, with obvious histopathological changes in liver. EGCG group significantly decreased the elevated the serum levels of AST and ALT and the mRNA levels of TLR4,TNF-a and IL-1β, the protein level of TLR4 and NF-κB P65 in left lobe of liver tissue, and lessened hepatic histopathological changes. Then, compared with I/R group, the levels of HO-1 mRNA/protein was significantly increase in EGCG group.Conclusion:EGCG can protect hepatic ischemia-reperfusion injury. The mechanism(s) underlying these effects of EGCG may involve the production of inflammatory factors of TLR4/NF-κB P65, HO-1, TNF-α、IL-6 and IL-1β expression.
Keywords/Search Tags:EGCG, HIRI, TLR4/NF-κB P65, HO-1, Balb/c mice
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