Therapeutic effects of Scutellaria baicalensis total flavonoids on metabolic syndrome in rats via modulation of PPARα and PPARγ signaling

IF 2.2 4区 生物学 Q3 CELL BIOLOGY
Yang Zhou, Zhi-Ping Li, Yu-Hang Lian, Xin Gao, Song-He Yin, Yu-Mei Zhao
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引用次数: 0

Abstract

The aim of this study is to evaluate the therapeutic effects of Scutellaria baicalensis total flavonoids (STF) in a rat model of metabolic syndrome (MS), with particular focus on the core regulatory mechanisms contributing to metabolic homeostasis. Additionally, the modulation of peroxisome proliferator-activated receptors (PPARs) by STF was investigated to elucidate its molecular targets and associated features within the pathophysiology of MS. Metabolic syndrome was induced in Sprague Dawley rats through the administration of a high-fat/high-glucose diet combined with streptozotocin (STZ). STF was administered orally during the induction period. Serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), fasting blood glucose (FBG), and fasting insulin (FINS) were quantified. The homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. Hepatic concentrations of TC and TG were also measured. Histopathological alterations were evaluated using hematoxylin and eosin (HE) staining, while hepatic lipid accumulation was assessed through Oil Red O staining. Hepatic expression levels of PPARα and PPARγ proteins were determined via Western blot analysis. Treatment with STF at doses of 50 and 100 mg·kg⁻¹ significantly reduced serum levels of TC, TG, LDL-C, FBG, FINS, and HOMA-IR, while preventing the decline in HDL-C levels among rats with MS. STF administration also alleviated abnormal liver weight and suppressed hepatic accumulation of TC and TG, accompanied by improvements in histological features. Western blot analysis revealed upregulation of hepatic PPARα and PPARγ protein expression following STF treatment. STF demonstrated the capacity to reduce body weight and improve lipid profiles and insulin resistance in rats with MS. These effects may be associated with the regulation of PPARα and PPARγ protein expression.

Abstract Image

Abstract Image

黄芩总黄酮通过调节PPARα和PPARγ信号通路对大鼠代谢综合征的治疗作用
本研究旨在评价黄芩总黄酮(STF)对代谢综合征(MS)大鼠模型的治疗作用,重点探讨其代谢稳态的核心调控机制。此外,研究了STF对过氧化物酶体增殖物激活受体(ppar)的调节作用,以阐明其在ms病理生理中的分子靶点和相关特征,并通过高脂/高糖饮食联合链脲佐菌素(STZ)诱导Sprague Dawley大鼠代谢综合征。诱导期口服STF。测定血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、空腹血糖(FBG)、空腹胰岛素(FINS)水平。计算胰岛素抵抗的稳态模型评估(HOMA-IR)。同时测定肝脏中TC和TG的浓度。采用苏木精和伊红(HE)染色评估组织病理学改变,油红O染色评估肝脏脂质积累。Western blot检测肝组织中PPARα和PPARγ蛋白的表达水平。用50和100 mg·kg剂量的STF治疗可以显著降低血清TC、TG、LDL-C、FBG、FINS和HOMA-IR的水平,同时阻止ms大鼠HDL-C水平的下降,STF还可以减轻肝脏异常重量,抑制肝脏TC和TG的积累,并伴有组织学特征的改善。Western blot分析显示,STF处理后肝脏PPARα和PPARγ蛋白表达上调。STF能够减轻ms大鼠的体重,改善脂质谱和胰岛素抵抗,这些作用可能与调节PPARα和PPARγ蛋白表达有关。
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来源期刊
Journal of Molecular Histology
Journal of Molecular Histology 生物-细胞生物学
CiteScore
5.90
自引率
0.00%
发文量
68
审稿时长
1 months
期刊介绍: The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.
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