Effects of PARP1 inhibitor PJ-34 on TGFα, IL-6, and IL-1β levels in diabetic nephropathy.

IF 3.6 3区 医学 Q2 IMMUNOLOGY
Jing Ke, Yanan Fan, Shaochun Zhang
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引用次数: 0

Abstract

Diabetic nephropathy is a severe chronic complication characterized by cytotoxicity, inflammation, and fibrosis, ultimately leading to renal failure. This study systematically investigated the effects of the PARP1 inhibitor PJ-34 on high glucose-induced cytotoxicity, inflammation, and fibrosis in HK-2 cells, as well as its improvement on neuropathic pain response and transforming growth factor β (TGFβ) expression in a type 1 diabetes mellitus diabetic nephropathy mouse model. Through cellular and animal experiments, we observed that PJ-34 significantly enhanced the proliferative capacity of cells damaged by high glucose, reduced apoptosis, and decreased the release of proinflammatory factors TGFα, interleukin-6, and interleukin-1β. In the type 1 diabetes mellitus nephropathy mouse model, the administration of PJ-34 substantially improved parameters of neuropathic pain, alleviated renal tissue damage, reduced indicators of renal functional impairment-inhibited renal fibrosis, and reduced the key protein expression in the epithelial-mesenchymal transition process, acting through the regulation of the TGFβ/Smads signaling pathway. This study elucidated the mechanism of action of the PARP1 inhibitor PJ-34 as a potential therapeutic agent for diabetic nephropathy, offering a novel strategy for its treatment.

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来源期刊
Journal of immunology
Journal of immunology 医学-免疫学
CiteScore
8.20
自引率
2.30%
发文量
495
审稿时长
1 months
期刊介绍: The JI publishes novel, peer-reviewed findings in all areas of experimental immunology, including innate and adaptive immunity, inflammation, host defense, clinical immunology, autoimmunity and more. Special sections include Cutting Edge articles, Brief Reviews and Pillars of Immunology. The JI is published by The American Association of Immunologists (AAI)
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