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投稿时间:2025-10-15
投稿时间:2025-10-15
中文摘要: 为探讨三七谷胱甘肽复合粉对衰老大鼠氧化应激和血管损伤的保护作用,将大鼠随机分为空白组、模型组、维生素E组、三七谷胱甘肽复合粉(Panax notoginseng-glutathione combination,PG)低、中、高剂量组,并采用D-半乳糖进行衰老造模。观测大鼠体质量、生命质量评分、脏器指数、颈动脉苏木精-伊红染色、血浆中纤维蛋白原含量和血小板最大聚集率、血清中氧化应激因子、炎症因子、血管损伤因子指标、肾组织中转化生长因子-β1(transforming growth factor-β1,TGF-β1)/Smad通路及相关蛋白表达水平。结果表明,与模型组相比,PG各剂量组能明显减缓衰老大鼠体质量的异常增加,降低生命质量评分,大鼠颈动脉壁变薄,血管腔变宽,纤维蛋白原(fibrinogen,FIB)含量和血小板最大聚集率降低,升高总超氧化物歧化酶(total superoxide dismutase,T-SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活力、6-酮-前列腺素F1α(6-keto-prostaglandin F1α,6-keto-PGF1α)含量,降低丙二醛(malondialdehyde,MDA)、一氧化氮/内皮素-1比值(nitric oxide/endothelin-1,NO/ET-1)、血栓素B2(thromboxane B2,TXB2)、白细胞介素-1β(interleukin-1β,IL-1β)、白细胞介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)含量;下调转化生长因子-β1(transforming growth factor-β1,TGF-β1)、磷酸化Smad2(phosphorylated Smad2,p-Smad2)、磷酸化Smad3(phosphorylated Smad3,p-Smad3)、I型胶原蛋白(collagen type I,Collagen I)与α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)表达水平,上调血管内皮生长因子-A(vascular endothelial growth factor A,VEGF-A)蛋白表达水平。综上,PG可通过抑制TGF-β1/Smad通路,增强机体抗氧化能力,减轻炎症反应与血管损伤,从而发挥对D-半乳糖致衰老大鼠血管损伤的保护作用。
Abstract:This study aimed to investigate the protective effect of Panax notoginseng-glutathione compound powder(PG)on oxidative stress and vascular injury in aging rats.In the experiment,rats were randomly divided into a blank group,a model group,a vitamin E group,and PG groups at low,medium,and high doses.An aging model was established by D-galactose.Then,aspects below were observed in the rats:body weight,quality of life scores,organ indexes,carotid artery hematoxylin and eosin(HE)staining,plasma fibrinogen content and maximum platelet aggregation rate,serum oxidative stress factor,inflammatory factor,and vascular injury factor indicators,as well as transforming growth factor-β1(TGF-β1)/Smad pathway and relevant protein expression levels in renal tissues.Results showed that,compared with the model group,manifestations below were significant in PG groups at all doses:alleviated abnormal body weight increase and decreased quality of life scores,thinner carotid wall,wider vascular lumen,decreased fibrinogen(FIB)content and maximum platelet aggregation rate,increased total superoxide dismutase(T-SOD)and glutathione peroxidase(GSH-Px)activities,as well as 6-keto-prostaglandin F1α(6-keto-PGF1α)content,decreased malondialdehyde(MDA),nitric oxide/endothelin-1(NO/ET-1),thromboxane B2(TXB2),interleukin-1β(IL-1β),interleukin-6(IL-6),and tumor necrosis factor-α(TNF-α)content,downregulated protein expression of transforming growth factor-β1(TGF-β1),phosphorylated Smad2(p-Smad2),phosphorylated Smad3(p-Smad3),collagen type I(Collagen I),and α-smooth muscle actin(α-SMA),as well as upregulated vascular endothelial growth factor A(VEGF-A)expression.In conclusion,PG could exert a protective effect against vascular injury in D-galactose-induced aging rats via inhibiting the TGF-β1/Smad pathway to enhance antioxidant capacity and alleviate inflammatory response and vascular damage.
文章编号:202605001 中图分类号: 文献标志码:
基金项目:国家重点研发计划项目(2018YFC1706803)
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