黄芪甲苷改善慢性肾小球肾炎大鼠肾功能,减轻肾损害和炎症。

Turkish journal of biology = Turk biyoloji dergisi Pub Date : 2022-12-09 eCollection Date: 2023-01-01 DOI:10.55730/1300-0152.2641
Dong Zhang, ZongYing Li, Yuan Gao, HaiLing Sun
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引用次数: 1

摘要

从黄芪(Fisch.)Bge.var.mongholicus(Bge.)Hsiao、黄芪甲苷IV(AS-IV)中可以纯化出一种皂苷,被认为是中药。本研究的目的是评估AS IV介导的慢性肾小球肾炎(CGN)的机制。建立阳离子牛血清白蛋白诱导的CGN大鼠模型,并给予10、15或20mg/kg的AS-IV以测量肾功能和炎症浸润。测定AS-IV对LPS诱导的大鼠系膜细胞(RMCs)增殖、细胞周期和炎症的影响。结果表明,AS-IV减轻了CGN大鼠的肾功能障碍、肾损伤和炎症。AS-IV延长RMCs的G0-G1期,缩短S期,并抑制细胞增殖和炎症。AS-IV可以促进miR-181d-5p的表达以抑制CSF1。miR-181d-5p的促进或CSF1的抑制可以进一步增强AS-IV在CGN大鼠中的治疗作用,而miR-181d-5 p的沉默或CSF1过表达消除了AS-IV的作用。总之,AS-IV通过介导miR-181d-5p/CSF1轴来保护CGN。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Astragaloside IV improves renal function and alleviates renal damage and inflammation in rats with chronic glomerulonephritis.

Astragaloside IV improves renal function and alleviates renal damage and inflammation in rats with chronic glomerulonephritis.

Astragaloside IV improves renal function and alleviates renal damage and inflammation in rats with chronic glomerulonephritis.

Astragaloside IV improves renal function and alleviates renal damage and inflammation in rats with chronic glomerulonephritis.

From Astragalus membranaceus (Fisch.) Bge.var. mongholicus (Bge.) Hsiao, astragaloside IV (AS-IV), a saponin can be purified and is considered traditional Chinese medicine. The purpose of this study was to evaluate the AS-IV-mediated mechanism on chronic glomerulonephritis (CGN). A cationic bovine serum albumin-induced CGN rat model was established and 10, 15, or 20 mg/kg of AS-IV was administered to measure renal function and inflammatory infiltration. Influences of AS-IV on proliferation, cell cycle, and inflammation of LPS-induced rat mesangial cells (RMCs) were determined. The results demonstrated that AS-IV alleviated renal dysfunction, renal lesions, and inflammation in CGN rats. AS-IV prolonged the G0-G1 phase, shortened the S phase, and inhibited cell proliferation and inflammation in RMCs. AS-IV can promote miR-181d-5p expression to inhibit CSF1. miR-181d-5p promotion or CSF1 suppression could further enhance the therapeutic role of AS-IV in CGN rats, while miR-181d-5p silencing or CSF1 overexpression abolished the effect of AS-IV. In conclusion, AS-IV by mediating the miR-181d-5p/CSF1 axis protects against CGN.

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