Effects of Rabdosia Rubescens on lipid metabolism in metabolism-associated fatty liver disease
MA Wenjun1 SHI Tingting2 BAI Minghui1 CHEN Xiaowei1 YANG Xingxin3▲
1.Department of Infectious Disease, Xixi Hospital of Hangzhou, Zhejiang Chinese Medical University, Zhejiang Province, Hangzhou 310023, China;
2.Department of Pharmaceutical Preparation, Xixi Hospital of Hangzhou, Zhejiang Chinese Medical University, Zhejiang Province, Hangzhou 310023, China; 3.College of Pharmaceutical Science, Yunnan University of Chinese Medicine, Yunnan Province, Kunming 650500, China
Abstract：Objective To investigate the effect of Rabdosia Rubescens on the expression of lipid metabolism-associated proteins in rats with metabolism-associated fatty liver disease (MAFLD). Methods The rats were fed with high-fat diet to replicate the metabolic-related fatty liver disease model. A total of 36 SD male rats were adaptively fed for one day, and they were divided into normal group, model group, and Rabdosia Rubescens low, medium, and high-dose groups by random number table method, each with six animals. The normal group was fed with ordinary feed, and the other groups were fed with high-fat feed. The low, medium, and high-doses of Rabdosia Rubescens were given 50, 100 mg/(kg·d) and 150 mg/(kg·d) per day, respectively; the normal group and the model group were given a gavage with the same volume of normal saline as the other experimental groups every day. HE staining was used to observe the degree of fatty degeneration of rat MAFLD liver tissue; automatic biochemical analyzer was used to detect triacylglycerol (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL- C), fasting blood glucose (FBG), fasting insulin (FINS); Western blot method was used to detect the expressions of peroxisome proliferator-activated receptor-α (PPAR-α), sterol regulatory element binding protein-1c (SREBP-1c), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) protein. Results The liver tissue of rats in the normal group showed clear and complete structure under microscope, the structure of liver lobules was normal, and the hepatocyte cords were neatly arranged. Hepatocyte damage in the model group showed diffuse hepatocyte steatosis with balloon-like hepatocytes, inflammatory cell infiltration in the portal area, and partial punctate hepatocyte necrosis and detrital necrosis. The degree of liver damage in the Rabdosia Rubescens high-dose group was significantly less than that of the model group. The fatty degeneration of hepatocytes was reduced. There was only a few punctate necrosis, a few fat droplets, and no obvious inflammatory cell infiltration in the portal area. The levels of TC, TG, HDL-C, LDL-C, FBG, and FINS of rats in each group were compared, and the differences were statistically significant (P ＜ 0.05). The levels of serum TC, TG, LDL-C, FBG, and FINS in the model group were higher than those in the normal group, while the level of HDL-C was lower than that in the normal group, and the differences were statistically significant (P ＜ 0.05). The content of TG and FINS in the low-dose Rabdosia Rubescens group were lower than those of the model group, and the differences were statistically significant (P ＜ 0.05); the content of TC, TG, LDL-C, FBG, and FINS in the medium-dose Rabdosia Rubescens group were lower than those of the model group, while TG and FBG were lower than those of the low-dose Rabdosia Rubescens group, and the differences were statistically significant (P ＜ 0.05). The content of TC, TG, LDL-C, FBG, and FINS in the high-dose Rabdosia Rubescens group were lower than those of the model group, while the level of HDL-C was higher than that of the model group, and TC, TG, LDL-C, FBG were lower than those of the low-dose Rabdosia Rubescens group, and the differences were statistically significant (P ＜ 0.05). The expressions of PPAR-α and ACC protein in the model group were lower than those of the normal group, while the expressions of SREBP-1c and FAS protein were higher than those of the normal group, and the differences were statistically significant (P ＜ 0.05). The expressions of PPAR-α and ACC protein in the low dose of Rabdosia Rubescens group were higher than those of the model group, while the expression of FAS protein was lower than that of the model group, and the differences were statistically significant (P ＜ 0.05). The expressions of PPAR-α and ACC protein in the medium and high-doses Rabdosia Rubescens group were higher than those of the model group and the low-dose Rabdosia Rubescens group, while the expressions of SREBP-1c and FAS protein were lower than those of the model group and the low-dose Rabdosia Rubescens group, and the differences were statistically significant (P ＜ 0.05). Conclusion Rabdosia Rubescens can regulate lipid metabolism and associated protein expression in rats with MAFLD, which lays a foundation for further study on the mechanism of the occurrence and development of MAFLD.
[1] 中华医学会肝病学分会脂肪肝和酒精性肝病学组，中国医师协会脂肪性肝病专家委员会.非酒精性脂肪性肝病防治指南（2018年版）[J].临床肝胆病杂志，2018，34（5）：947-957.
[2] Wang FS，Fan JG，Zhang Z，et al. The global burden of liver disease：the major impact of China [J]. Hepatology，2014， 60（6）：2099-2108.
[3] Cotter TG，Rinella M. Nonalcoholic Fatty Liver Disease 2020：The State of the Disease[J]. Gastroenterology，2020，158（7）：1851-1864.
[4] Miao M，Yan X，Guo L，et al. Effects of the Rabdosia rubescens total flavonoids on focal cerebral ischemia reperfusion model in rats [J]. Saudi Pharm J，2017，25（4）：606-614.
[5] 吴岚，包丽萍，李菊霜，等.冬凌草甲素通过调节氧化应激和脂代谢减轻糖尿病大鼠肾损伤[J].临床肾脏病杂志，2017，17（11）：692-696.
[6] Bedossa P. Utility and appropriateness of the fatty liver inhibition of progression（FLIP）algorithm and steatosis，activity，and fibrosis（SAF）score in the evaluation of biopsies of nonalcoholic fatty liver disease [J]. Hepatology，2014，60（2）：565-575.
[7] Eslam M，Sanyal AJ，George J，et al. MAFLD：A Consensus-Driven Proposed Nomenclature for Metabolic Associated Fatty Liver Disease [J]. Gastroenterology，2020，158（7）：1999-2014.
[8] Shi TT，Wu L，Ma WJ，et al. Nonalcoholic Fatty Liver Disease：Pathogenesis and Treatment in Traditional Chinese Medicine and Western Medicine [J]. Evid Based Complement Alternat Med，2020，2020：8749564.
[9] Alwahsh SM，Gebhardt R. Dietary fructose as a risk factor for non-alcoholic fatty liver disease（NAFLD）[J]. Arch Toxicol，2017，91（4）：1545-1563.
[10] European Association for the Study of the Liver（EASL），European Association for the Study of Diabetes（EASD），European Association for the Study of Obesity（EASO）. EASL-EASD-EASO Clinical Practice Guidelines for the management of non-alcoholic fatty liver disease [J]. Diabetologia，2016，59（6）：1121-1140.
[11] Shi TT，Yang XX，Zhou HP，et al. Activated Carbon N-acetylcysteine Microcapsule Protects Against Nonalcoholic Fatty Liver Disease in Young Rats via Activating Telomerase and Inhibiting Apoptosis [J]. PLoS One，2018，13（1）：e0189856.
[12] Lau LHS，Wong SH. Microbiota，Obesity and NAFLD [J]. Adv Exp Med Biol，2018，1061：111-125.
[13] Liermann J，Naumann P，Fortunato F，et al. Phytotherapeutics oridonin and ponicidin show additive effects combined with irradiation in pancreatic cancer in vitro [J]. Radiol Oncol，2017，51（4）：407-414.
[14] Bae S，Lee EJ，Lee JH，et al. Oridonin protects HaCaT keratinocytes against hydrogen peroxide-induced oxidative stress by altering microRNA expression [J]. Int J Mol Med，2014，33（1）：185-193.
[15] Li Y，Wang Y，Wang S，et al. Oridonin phosphate-induced autophagy effectively enhances cell apoptosis of human breast cancer cells [J]. Med Oncol，2015，32（1）：365.
[16] Ding Y，Ding C，Ye N，et al. Discovery and development of natural product oridonin-inspired anticance agents [J]. Eur J Med Chem，2016，122（10）：102-117.
[17] 成伯宁，刘殿雷，史婷婷，等.冬凌草对非酒精性脂肪肝大鼠氧化应激及脂肪酸代谢的影响[J].中国临床药理学杂志，2020，36（10）：1252-1255.
[18] He HB，Jiang H，Chen Y，et al. Oridonin Is a Covalent NLRP3 Inhibitor With Strong Anti-Inflammasome Activity [J]. Nat Commun，2018，9（1）：2550.
[19] 宋琪雯，刘智，孙为民，等.冬凌草对酒精性肝损伤模型大鼠炎性因子及肝功能的影响[J].中国生化药物杂志，2015，10（35）：15-21.
[20] 王宫，魏文增，吴华蒿.牛樟芝滴丸对大鼠非酒精性脂肪肝的干预作用[J].福建中医，2018，49（4）：41-43.
[21] López-Sánchez GN，Dóminguez-Pérez M，Uribe M，et al. Non-alcoholic fatty liver disease and microRNAs expression，how it affects the development and progression of the disease [J]. Ann Hepatol，2020：S1665-2681（20）30053-3.
[22] 张方.与肝脏脂质代谢异常相关的转录因子的研究进展[J].现代临床医学，2014，40（3）：163-166.
[23] Kersten S. Peroxisom proliferator activated receptors and obesity [J]. Eur J Pharmacol，2002，440（2/3）：223-234.
[24] 魏文增，王宫，吴华嵩.牛樟芝滴丸对大鼠非酒精性脂肪肝相关基因表达的影响[J].中国中医药科技，2020， 27（2）：186-189.
[25] Torres JL，Novo-Veleiro I，Manzanedo L，et al. Role of microRNAs in alcohol-induced liver disorders and non-alcoholic fatty liver disease [J]. World J Gastroenterol，2018，24（36）：4104-4118.
2020, Vol. 17 
京公网安备 11010502046598号