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来自[具体来源未给出]的皂苷可减轻高脂饮食诱导的肥胖小鼠的脂肪组织纤维化和代谢功能障碍。

Saponins from alleviate adipose tissue fibrosis and metabolic dysfunction in high-fat-diet-induced obese mice.

作者信息

Hu Xiaoqin, Sun Ao, Chen Huijian, Yan Xiyue, Ding Fei, Zheng Peng, Li Zhen, Yan You-E

机构信息

Department of Pharmacology, School of Basic Medical Sciences, Wuhan University, Wuhan, China.

Department of Hepatobiliary and Pancreatic Surgery, Zhongnan Hospital, Wuhan University, Wuhan, China.

出版信息

Biomarkers. 2022 Dec;27(8):784-794. doi: 10.1080/1354750X.2022.2122566. Epub 2022 Sep 15.

DOI:10.1080/1354750X.2022.2122566
PMID:36083032
Abstract

INTRODUCTION

Adipose tissue fibrosis is a typical feature of adipose tissue dysfunction in obese individuals, which is closely related to metabolic diseases.

OBJECTIVE

To explore the effect and mechanism of Saponins from (SPJ) on adipose tissue fibrosis in obese mice induced by high fat diet (HFD).

MATERIALS AND METHODS

We established a HFD induced obese mice model. Then the obese mice were treated with 90 mg/kg SPJ by oral gavage for 10 weeks. The levels of adipose tissue fibrosis and molecules related to signalling pathways were measured. Then the effects of SPJ on TGFβ1-induced fibrosis in 3T3-L1 differentiated adipocytes were evaluated.

RESULTS

SPJ reduced body weight, fat accumulation, and improved glucose and lipid metabolism in obese mice. SPJ decreased collagen deposition and expressions of fibrotic genes in epididymal white adipose tissue (eWAT) of obese mice. SPJ decreased the levels of TGFβ1 protein and pSmad2, and increased the expression of PPARγ and PGC1α, thus alleviating oxidative stress in eWAT. Consistently, SPJ inhibited TGFβ1-induced fibrosis in 3T3-L1 differentiated adipocytes.

CONCLUSIONS

SPJ may alleviate adipose tissue fibrosis and improve obesity by inhibiting TGFβ1/Smad2 and activating PPARγ/PGC1α pathway. SPJ is expected to become an efficient medicine for treatment of obesity.

摘要

引言

脂肪组织纤维化是肥胖个体脂肪组织功能障碍的典型特征,与代谢性疾病密切相关。

目的

探讨绞股蓝总皂苷(SPJ)对高脂饮食(HFD)诱导的肥胖小鼠脂肪组织纤维化的影响及机制。

材料与方法

建立HFD诱导的肥胖小鼠模型。然后对肥胖小鼠进行为期10周的灌胃给药,剂量为90mg/kg SPJ。检测脂肪组织纤维化水平及与信号通路相关的分子。然后评估SPJ对3T3-L1分化脂肪细胞中TGFβ1诱导的纤维化的影响。

结果

SPJ降低了肥胖小鼠的体重、脂肪堆积,改善了葡萄糖和脂质代谢。SPJ减少了肥胖小鼠附睾白色脂肪组织(eWAT)中的胶原沉积和纤维化基因的表达。SPJ降低了TGFβ1蛋白和pSmad2的水平,增加了PPARγ和PGC1α的表达,从而减轻了eWAT中的氧化应激。同样,SPJ抑制了3T3-L1分化脂肪细胞中TGFβ1诱导的纤维化。

结论

SPJ可能通过抑制TGFβ1/Smad2和激活PPARγ/PGC1α通路减轻脂肪组织纤维化并改善肥胖。SPJ有望成为治疗肥胖的有效药物。

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