小紫薇醇提物的抗肥胖活性研究。(叶)Wistar白化大鼠模型

C. Tyagi
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引用次数: 0

摘要

目的:评价小花紫薇醇提物的抗肥胖作用。(MELPR)(叶片)在高热量饮食(HCD)诱导的肥胖Wistar白化大鼠中的表达。材料与方法:小檗属植物提取物。用不同的溶剂对其脂肪酶抑制活性进行了评价。采用不同浓度(200和300 mg/kg体重[b.w.])的MELPR口服,评估生化指标(血清谷氨酸丙酮酸转氨酶[SGPT]和碱性磷酸酶])、皮肤和行为活性、口服葡萄糖耐量试验(OGTT)、极低密度脂蛋白(VLDL)和低密度脂蛋白(LDL)胆固醇(VLDL- c和LDL- c)以及抗肥胖潜力。同时进行组织病理学评价。结果与讨论:正己烷提取物对胰脂肪酶(PL)无抑制作用,甲醇提取物对胰脂肪酶(PL)有75%的抑制作用。血液学研究表明,治疗组血红蛋白浓度明显高于对照组。生化研究结果表明,与对照组相比,治疗组肌酐和尿素水平略有下降。OGTT结果数据显示,与正常对照大鼠相比,HCD控制的肥胖大鼠血糖、胰岛素和胰岛素抵抗显著(P < 0.05)升高。抗肥胖活动数据表明,HCD在生理生化方面发生了实质性的改变。施用MELPR显著降低体重、总脂肪、脂肪百分比、血糖、胰岛素抵抗和血脂,呈剂量依赖性(200和300 mg/kg体重)。结论:MELPR在3000 mg/kg体重下对大鼠无毒、安全。其他研究也支持MELPR治疗对hcd诱导的肥胖、高脂血症具有剂量依赖性和显著性缓解作用。本研究证实了MELPR的降血脂和抗肥胖潜力,为开发抗肥胖药物提供了科学验证和依据。
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Antiobesity activity of methanolic extract of Lagerstroemia parviflora Roxb. (leaves) on Wistar albino rat model
Objective: The objective of research paper is to evaluate the antiobesity potential of methanolic extract of Lagerstroemia parviflora Roxb. (MELPR) (leaves) in obese Wistar albino rats induced with high-calorie diet (HCD). Materials and Methods: The plant extract of L. parviflora Roxb. (leaves) with different solvents was evaluated for the lipase inhibitory activity. The MELPR at different concentrations (200 and 300 mg/kg body weight [b.w.]) was administered orally and evaluated for the estimation of biochemical parameters (serum glutamate pyruvate transaminase [SGPT] and alkaline phosphatase), skin and behavioral activity, oral glucose tolerance test (OGTT) and very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) cholesterol (VLDL-C and LDL-C), and antiobesity potential. Histopathological evaluation was also performed. Results and Discussion: The pancreatic lipase (PL) inhibitory activity result indicated that hexane extract did not inhibit the PL, whereas methanolic extract showed 75% inhibitory activity. Hematological study indicates that hemoglobin concentration was increased in treated group compared to control group. Biochemical study results indicate that creatinine and urea levels were found to be little lowering in treated groups compared to control group. OGTT result data indicate a significant (P < 0.05) elevation in plasma glucose, insulin, and insulin resistance in HCD control obese rats when compared to normal control rats. The antiobesity activities data indicate that HCD has substantially altered physiological and biochemical aspects. Administration of MELPR reduced significantly, b.w., total fat, fat percentage, blood glucose, insulin resistance, and lipid profile in a dose-dependent manner (200 and 300 mg/kg b.w.). Conclusion: The MELPR is non-toxic and safe up to 3000 mg/kg bodyweight in rats. Treatment with MELPR has dose dependently and significantly alleviated HCD-induced obesity, hyperlipidemia, as supported by other studies. This study demonstrates the antihyperlipidemic and antiobesity potential of MELPR and offers scientific validation and basis to develop antiobesity drugs.
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