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游泳运动通过减轻肾间质纤维化和细胞凋亡改善高血压引起的肾脏功能障碍。

Swimming Exercise Ameliorates Hypertension-Induced Kidney Dysfunction via Alleviating Renal Interstitial Fibrosis and Apoptosis.

机构信息

School of Physical Education, Shaanxi Normal University, Xi'an, China.

School of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an, China.

出版信息

Kidney Blood Press Res. 2021;46(2):219-228. doi: 10.1159/000514680. Epub 2021 Apr 13.

Abstract

BACKGROUND

Hypertensive nephropathy is one of the major causes of ESRD. Exercise has been considered a nonpathological therapy for hypertension and its complications, yet mechanisms remain unclear. We sought to investigate whether periodic swimming could ameliorate hypertension-induced kidney dysfunction and its underlying mechanisms.

METHODS

Four-week male spontaneously hypertensive rats (SHRs) were randomly divided into the hypertension group (SHR, n = 8) and exercise group (SE, n = 8, 60 min swimming/day, 6 days per week, for 8 weeks). Wistar-Kyoto rats (WKY, n = 8) were served as a sedentary normotensive group. Bodyweight and blood pressure (BP) were recorded weekly. After 8-week sedentary or swimming exercise, lipids profile, BUN, and Cr were measured. The renal interstitial fibrosis was examined by the histopathological analysis using Masson's trichrome staining and hematoxylin and eosin staining. The kidney cell apoptosis was tested by TUNEL staining. The expressions of critical proteins responsible for the TGF-β1/Smad signaling of fibrosis, that is, TGF-β1, Smad2/3, and Smad7, as well as apoptosis related proteins, Bax and Bcl-2 in kidney cortex tissues were measured.

RESULTS

The 8-week swimming exercise reduced BP and bodyweight, lowered concentrations of BUN, and serum Cr, compared with SHR. Exercise remarkably inhibited hypertension-induced tubular degeneration, cellular cluster, and tubular cell swelling as well as glomerular degeneration in the kidney cortical tissues, attenuated renal interstitial fibrosis, and renal cell apoptosis. Moreover, expressions of TGF-β1, Smad2/3, and Bax were higher in the SHR than the WKY, which were significantly suppressed by the exercise. In contrast, hypertension-reduced expressions of Smad7 and Bcl-2 were enhanced by the swimming exercise. Strong correlations were found between kidney function indices, blood lipids, and key protein expressions.

CONCLUSION

Our results demonstrate beneficial effects of the periodic swimming on ameliorating hypertension-induced kidney dysfunction highlighting the potential of swimming exercise as a nonpathological therapy for early prevention of hypertension-caused kidney diseases.

摘要

背景

高血压肾病是终末期肾病的主要原因之一。运动被认为是治疗高血压及其并发症的一种非病理性疗法,但机制尚不清楚。我们试图研究定期游泳是否可以改善高血压引起的肾功能障碍及其潜在机制。

方法

将四周龄雄性自发性高血压大鼠(SHR)随机分为高血压组(SHR,n=8)和运动组(SE,n=8,每天游泳 60 分钟,每周 6 天,共 8 周)。Wistar-Kyoto 大鼠(WKY,n=8)作为久坐的正常血压组。每周记录体重和血压(BP)。经过 8 周的久坐或游泳运动后,测量血脂谱、BUN 和 Cr。通过 Masson 三色染色和苏木精-伊红染色的组织病理学分析检查肾间质纤维化。通过 TUNEL 染色检测肾细胞凋亡。测量肾脏皮质组织中负责 TGF-β1/Smad 信号转导纤维化的关键蛋白,即 TGF-β1、Smad2/3 和 Smad7,以及凋亡相关蛋白 Bax 和 Bcl-2 的表达。

结果

8 周游泳运动降低了 SHR 的血压和体重,降低了 BUN 和血清 Cr 的浓度。运动显著抑制了高血压引起的肾小管变性、细胞簇和肾小管细胞肿胀以及肾小球皮质组织的退行性变,减轻了肾间质纤维化和肾细胞凋亡。此外,SHR 中 TGF-β1、Smad2/3 和 Bax 的表达高于 WKY,运动显著抑制了它们的表达。相反,高血压降低的 Smad7 和 Bcl-2 的表达被游泳运动增强。肾脏功能指标、血脂和关键蛋白表达之间存在很强的相关性。

结论

我们的结果表明,定期游泳对改善高血压引起的肾功能障碍有有益的影响,强调了游泳运动作为预防高血压引起的肾脏疾病的一种非病理性治疗的潜力。

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