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The Therapeutical Effect And Mechanism Of Traditional Mongolian Medicine "San Gen Tiao Jie Fa" On Non-alcoholic Fatty Liver Disease In Rats

Posted on:2012-02-16Degree:MasterType:Thesis
Country:ChinaCandidate:H P TianFull Text:PDF
GTID:2154330335977409Subject:Pharmacology
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Object:According to traditional Mongolian medicine theory "San gen tiao jie fa" relieving "Xila", suppressing "Heyi" and driving "Badagan" out, we selected three representative prescription-Digeda-4, LiGanShiLiuBaweisan and Tonglaga-5, and observed their effect on non-alcoholic fatty liver disease (NAFLD) in rats. We're trying to explore the mechanism of "San gen tiao jie fa" curing NAFLD.Method:Non-alcoholic fatty liver disease rat model was successfully established by feeding fatty milk. The rats were randomly divided into six groups including control, model, positive control, Digeda-4, LiGanShiLiuBaweisan and Tonglaga-5 groups. Blood were collected and livers were quickly excised from rats after being treated with drugs for 4 weeks.1. serum TG, TC, HDL-C, LDL-C, FFA, AST, ALT, FBS, FINS levels and FIRI were detected, and tissue TG, TC levels, SOD activity, MDA content were also detected; 2. Histomorphology changes of hepatic tissue in rats were observed (HE and Oil red staining); 3. LXRamRNA, PPARamRNA and PPARymRNA expression were detected by Real time PCR analysis; 4. LXRa, PPARa and PPARy protein expression were observed by Immunohistochemistry analysis.Results:(1) Be treated with Digeda-4, the rat serum TG, LDL-C, FFA, AST, FINS levels and FIRI were decreased compared with the model group. The tissue TG, TC levels and MDA content in liver were also decreased; Be treated with LiGanShiLiuBaweisan, the rat serum TG, LDL-C, FFA, AST, FINS levels and FIRI were decreased compared with the model group. The tissue TG, TC levels and MDA content in liver were also decreased, while the tissue SOD activity were increased; Be treated with Tonglaga-5 the rat serum TG, TC, LDL-C, FFA, AST, FINS levels and FIRI were decreased with the model group. The tissue TG, TC levels and MDA content were also decreased, while the tissue SOD activity was increased.(2) HE staining and red oil staining showed that the histomorphology changes of hepatic tissue in NAFLD rats were improved in a certain extent after being treated with Digeda-4, LiGanShiLiuBaweisan and Tonglaga-5.(3) Real time PCR analysis showed that the hepatic tissue LXRamRNA expression was significantly decreased, while PPARa/ymRNA expression were obviously enhanced after being treated with Digeda-4; And the hepatic tissue LXRamRNA expression was also significantly decreased, while PPARa/ymRNA expression were obviously enhanced after being treated with LiGanShiLiuBaweisan; Only the hepatic tissue LXRamRNA expression was significantly decreased after being treated with Tonglaga-5, but PPARa/ymRNA expression were not changed.(4) Immunohistochemistry analysis showed that the hepatic tissue LXRa protein expression was decreased, PPARy protein was increased, but PPARa protein was not impacted after being treated with Digeda-4; The hepatic tissue LXRa protein expression was decreased, PPARa protein was increased, but PPARy protein was not impacted after being treated with LiGanShiLiuBaweisan; The hepatic tissue LXRa protein expression was decreased, PPARa protein was increased, but PPARy protein was not impacted after being treated with Tonglaga-5.Conclusion:The three therapy principal which Digeda-4, LiGanShiLiuBaweisan and Tonglaga-5 represented, including suppressing "Heyi", relieving "Xila" and driving "Badagan" out possesses the features that decreasing serum lipid, improving liver function, anti-oxidation, and modifying insulin resistance in NAFLD rats, the mechanism may be associated with controlling LXRa and PPARs genes and protein expression; The biological meaning of "Heyi", "Xila" and "Badagan" is partially related to the physiological effect of LXRa and PPARs.
Keywords/Search Tags:traditional Mongolian medicine, non-alcoholic fatty liver disease, Digeda-4, LiGanShiLiuBaweisan, Tonglaga-5, peroxisome proliferators-activated receptor, Liver X receptor
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