Inhibition of Pyroptosis of Renal Tubular Epithelial Cells by Puerarin via Regulation of lncRNA NEAT1 Ameliorating Chronic Renal Failure.

IF 0.8 4区 医学 Q4 UROLOGY & NEPHROLOGY
Iranian journal of kidney diseases Pub Date : 2024-01-01
Jing Yang, Baochao Li, Jiangming Wang, Wenxing Fan
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引用次数: 0

Abstract

Introduction: Chronic kidney disease (CKD) is one of the major chronic human diseases worldwide. Puerarin, extensively used in traditional Chinese medicine, has shown favorable clinical effects in treating CKD. Here, we aimed to elucidate the mechanism by which puerarin alleviates CKD.

Methods: We constructed an animal model of CKD and intragastrically administered 400 mg/kg puerarin to the rat models. The extent of kidney injury was evaluated by performing hematoxylin and eosin staining. Then, we quantified the renal function indicators, inflammatory cytokines, apoptosis-related factors, and pyroptosis-related factors. HK-2 cells were treated with lipopolysaccharide (400 ng/mL) in H2O2 (200 μM) to induce oxidative stress. Then, the cells were treated with puerarin and transfected with overexpressed lncRNA NEAT1 vectors. Finally, the regulatory functions of lncRNA NEAT1 in cell apoptosis and pyroptosis were investigated.

Results: Puerarin treatment alleviated kidney damage and suppressed inflammation and apoptosis in the CKD rat model. Puerarin ameliorated pyroptosis in the CKD model by inhibiting caspase-1 and GSDMD-N expression. LncRNA NEAT1 was down-regulated in the CKD model after puerarin treatment. Puerarin enhanced cell viability when lncRNA NEAT1 was overexpressed, and the inhibition of apoptosis was reversed in the LPS/H2O2-stimulated HK-2 cells. Furthermore, lncRNA NEAT1 overexpression blocked the anti-pyroptosis effect of Puerarin in the CKD model.

Conclusion: Puerarin inhibits pyroptosis and inflammation by regulating lncRNA NEAT1, thereby ameliorating CKD.  DOI: 10.52547/ijkd.7565.

葛根素通过调控lncRNA NEAT1抑制肾小管上皮细胞的脓毒症改善慢性肾衰竭
简介慢性肾脏病(CKD)是全球人类主要慢性疾病之一。葛根素被广泛应用于传统中药,在治疗 CKD 方面显示出良好的临床效果。在此,我们旨在阐明葛根素缓解 CKD 的机制:方法:我们构建了一个 CKD 动物模型,并给大鼠胃内注射了 400 mg/kg 葛根素。通过苏木精和伊红染色评估肾损伤程度。然后,我们对肾功能指标、炎症细胞因子、细胞凋亡相关因子和热解相关因子进行了量化。用脂多糖(400 ng/mL)和H2O2(200 μM)处理HK-2细胞以诱导氧化应激。然后,用葛根素处理细胞并转染过表达的 lncRNA NEAT1 载体。最后,研究了lncRNA NEAT1在细胞凋亡和热凋亡中的调控功能:结果:葛根素能减轻 CKD 大鼠模型的肾损伤,抑制炎症和细胞凋亡。葛根素通过抑制caspase-1和GSDMD-N的表达,改善了CKD模型的脓毒症。葛根素治疗后,LncRNA NEAT1在CKD模型中下调。当lncRNA NEAT1过表达时,葛根素可增强细胞活力,而在LPS/H2O2刺激的HK-2细胞中,葛根素对细胞凋亡的抑制作用被逆转。此外,lncRNA NEAT1的过表达阻断了葛根素在CKD模型中的抗脓毒症作用:结论:葛根素通过调控lncRNA NEAT1抑制脓毒症和炎症反应,从而改善CKD。 DOI: 10.52547/ijkd.7565.
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来源期刊
Iranian journal of kidney diseases
Iranian journal of kidney diseases UROLOGY & NEPHROLOGY-
CiteScore
2.50
自引率
0.00%
发文量
43
审稿时长
6-12 weeks
期刊介绍: The Iranian Journal of Kidney Diseases (IJKD), a peer-reviewed journal in English, is the official publication of the Iranian Society of Nephrology. The aim of the IJKD is the worldwide reflection of the knowledge produced by the scientists and clinicians in nephrology. Published quarterly, the IJKD provides a new platform for advancement of the field. The journal’s objective is to serve as a focal point for debates and exchange of knowledge and experience among researchers in a global context. Original papers, case reports, and invited reviews on all aspects of the kidney diseases, hypertension, dialysis, and transplantation will be covered by the IJKD. Research on the basic science, clinical practice, and socio-economics of renal health are all welcomed by the editors of the journal.
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