Effects of Dihydromyricetin from Guangxi Vine Tea on Hepatocelluar Apoptosis in Mice
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Effects of Dihydromyricetin from Guangxi Vine Tea on Hepatocelluar Apoptosis in Mice
Chinese Journal of Experimental Traditional Medical FormulaeVol. 16, Issue 16, Pages: 102-104(2010)
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Published:2010
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YAN Li, WEI Zhi-quan, ZHENG Zuo-wen, et al. Effects of Dihydromyricetin from Guangxi Vine Tea on Hepatocelluar Apoptosis in Mice[J]. Chinese journal of experimental traditional medical formulae, 2010, 16(16): 102-104.
DOI:
YAN Li, WEI Zhi-quan, ZHENG Zuo-wen, et al. Effects of Dihydromyricetin from Guangxi Vine Tea on Hepatocelluar Apoptosis in Mice[J]. Chinese journal of experimental traditional medical formulae, 2010, 16(16): 102-104.DOI:
Effects of Dihydromyricetin from Guangxi Vine Tea on Hepatocelluar Apoptosis in Mice
Objective: To study the inhibitory effect of dihydromyricetin from Ampelopsis grossedentata (Hand-Mazz) W.T. Wang (Vine tea dihydromyricetin
VTD) on hepatocyte apoptosis induced by the cessation of phenobarbital sodium (SP) injection treatment in mice
and to explore its mechanism of hepatoprotective effect. Method: The mouse model with hepatocellular apoptosis induced by removing SP was established.The mice were randomly divided into blanks
negative controls
positive controls and test groups.Test groups of mice were given intragastric gavage of 200
50 mg ·kg-1 VTD.Hepatic apoptosis was detected by flow cytometry
and pathological changes in the liver tissue were observed after HE staining. Result: The histopathological analysis of the liver showed normal liver morphology in blanks and negative controls
and varying degrees of liver cell apoptosis in positive controls and low- and high-dose VTD groups.The outcome from flow cytometry and TUNEL showed hepatocelluar apoptosis rate in low dose of VTD group were 17.7%
2.9% respectively.All of these values were lower than those in positive controls (P<0.01). Conclusion: The mouse hepatocellular apoptosis induced by removing SP can be markedly inhibited by treating with VTD in 50 mg ·kg-1
and it might be one of the hepatoprotective mechanisms for VTD to inhibit the hepatocelluar apoptosis.