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理中汤对大鼠非酒精性脂肪性肝病的保护作用及机制。

Protective effects and mechanisms of Lizhong decoction against non-alcoholic fatty liver disease in a rat model.

机构信息

Department of Gastroenterology, Wuhan Integrated TCM and Western Medicine Hospital, Wuhan 430022, China.

Department of Endocrinology, The Third People's Hospital of Hubei Province, Wuhan 430033, China.

出版信息

J Tradit Chin Med. 2022 Oct;42(5):773-780. doi: 10.19852/j.cnki.jtcm.2022.05.009.

DOI:10.19852/j.cnki.jtcm.2022.05.009
PMID:36083485
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9924662/
Abstract

OBJECTIVE

To investigate the protective effects and molecular mechanisms of Lizhong decoction (, LZD) against non-alcoholic fatty liver disease (NAFLD).

METHODS

Male Wistar rats were fed a high-fat diet for four weeks to induce NAFLD, and were administered LZD by gavage for four weeks. Potential therapeutic targets for NAFLD were analyzed using network pharmacology. Liver pathology was evaluated using Oil Red O and hematoxylin-eosin staining. Furthermore, mitochondrial function, lipid metabolism, oxidative stress, and inflammatory response were examined.

RESULTS

Rats with NAFLD exhibited high levels of hepatic damage and cholesterol deposition. Moreover, apoptosis was increased, superoxide dismutase and glutathione content were reduced, malondialdehyde content was increased, and the protein expression of inflammatory cytokines and p-c-Jun N-terminal kinase was increased. The LZD treatment ameliorated mitochondrial dysfunction, reduced liver damage, inhibited oxidative stress and inflammatory response, upregulated peroxisome proliferator-activated receptor (PPAR)-γ expression, and suppressed dipeptidyl peptidase 4 (DPP4) expression in the liver.

CONCLUSION

It was found that LZD alleviates NAFLD by activating PPAR-γ and inhibiting DPP4.

摘要

目的

探讨理中汤(LZD)防治非酒精性脂肪性肝病(NAFLD)的作用及其分子机制。

方法

雄性 Wistar 大鼠给予高脂饮食 4 周诱导 NAFLD,并用灌胃给予 LZD 4 周。采用网络药理学分析 NAFLD 的潜在治疗靶点。油红 O 和苏木精-伊红染色评估肝组织病理。进一步检测线粒体功能、脂质代谢、氧化应激和炎症反应。

结果

NAFLD 大鼠肝损伤和胆固醇沉积明显升高,凋亡增加,超氧化物歧化酶和谷胱甘肽含量降低,丙二醛含量增加,炎症细胞因子和 p-c-Jun N-末端激酶的蛋白表达增加。LZD 治疗可改善线粒体功能障碍,减轻肝损伤,抑制氧化应激和炎症反应,上调过氧化物酶体增殖物激活受体(PPAR)-γ的表达,并抑制肝脏中二肽基肽酶 4(DPP4)的表达。

结论

LZD 通过激活 PPAR-γ和抑制 DPP4 缓解 NAFLD。

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