Isorhapontigenin ameliorates high glucose-induced podocyte and vascular endothelial cell injuries via mitigating oxidative stress and autophagy through the AMPK/Nrf2 pathway

Tian, Hanqin; Zheng, Xiang; Wang, Hui

doi:10.1007/s11255-022-03325-y

Cited by 9 publications

(6 citation statements)

References 41 publications

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“…Renal damage by CoCl 2 toxicity was further corroborated by an exaggerated increase in serum BUN and creatinine. A recent study revealed a positive correlation between renal damage and heightened levels of BUN and creatinine 48 . Therefore, the observed decrease in the expression of podocin in renal tissues of rats treated with glycine in this study suggests a preservation of the structural integrity of renal tissues and therefore indicates that glycine is a potent renoprotective agent against renal toxicities associated with CoCl 2 exposures.…”

Section: Discussionsupporting

confidence: 65%

“…A recent study revealed a positive correlation between renal damage and heightened levels of BUN and creatinine. 48 Therefore, the observed decrease in the expression of podocin in renal tissues of rats treated with glycine in this study suggests a preservation of the structural integrity of renal tissues and therefore indicates that glycine is a potent renoprotective agent against renal toxicities associated with CoCl 2 exposures. Recent experimental studies also confirmed high expression of podocin as a novel biomarker of renal damage during acute kidney injury.…”

Section: Discussionmentioning

confidence: 54%

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Ameliorative effects of glycine on cobalt chloride‐induced hepato‐renal toxicity in rats

Iji¹,

Ajibade

Esan

et al. 2023

Anim Models and Exp Med

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Background:The important roles of liver and kidney in the elimination of injurious chemicals make them highly susceptible to the noxious activities of various toxicants including cobalt chloride (CoCl 2 ). This study was designed to investigate the role of glycine in the mitigation of hepato-renal toxicities associated with CoCl 2 exposure.Methods: Forty-two (42) male rats were grouped as Control; (CoCl 2 ; 300 ppm);CoCl 2 + Glycine (50 mg/kg); CoCl 2 + Glycine (100 mg/kg); Glycine (50 mg/kg); and Glycine (100 mg/kg). The markers of hepatic and renal damage, oxidative stress, the antioxidant defense system, histopathology, and immunohistochemical localization of neutrophil gelatinase associated lipocalin (NGAL) and renal podocin were evaluated.Results: Glycine significantly reduced the markers of oxidative stress (malondialdehyde content and H 2 O 2 generation), liver function tests (ALT, AST, and ALP), markers of renal function (creatinine and BUN), and decreased the expression of neutrophil gelatinase-associated lipocalin (NGAL) and podocin compared with rats exposed to CoCl 2 toxicity without glycine treatment. Histopathology lesions including patchy tubular epithelial necrosis, tubular epithelial degeneration and periglomerular inflammation in renal tissues, and severe portal hepatocellular necrosis, inflammation, and duct hyperplasia were observed in hepatic tissues of rats exposed to CoCl 2 toxicity, but were mild to absent in glycine-treated rats. Conclusion:The results of this study clearly demonstrate protective effects of glycine against CoCl 2 -induced tissue injuries and derangement of physiological activities of the hepatic and renal systems in rats. The protective effects are mediated via augmentation of total antioxidant capacity and upregulation of NGAL and podocin expression.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 54%

Ameliorative effects of glycine on cobalt chloride‐induced hepato‐renal toxicity in rats

Iji¹,

Ajibade

Esan

et al. 2023

Anim Models and Exp Med

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“…In turn, autophagy of podocytes plays a renoprotective role against DKD related structural endothelial injury ( 110 ). Activating the AMPK pathway was proved to improve the renal injury of DKD by improving autophagy of GECs ( 29 , 111 ), suggesting the important role of autophagy of GECs in improving DKD.…”

Section: Autophagy and Renal Homeostasismentioning

confidence: 99%

“…Fisetin has also been found to reduce podocyte injury in DN by restoring autophagy and inhibiting the NLRP3 inflammasome ( 147 ). Isorhapontigenin attenuates HG-induced oxidative stress and activates autophagy by stimulating AMPK/Nrf2 pathway, thereby improving the EndMT and podocyte injury of DKD ( 111 ).…”

Section: Polyphenols Used To Regulate Autophagy In Dkdmentioning

confidence: 99%

Regulation of autophagy by natural polyphenols in the treatment of diabetic kidney disease: therapeutic potential and mechanism

Liu,

Jin,

Yang

et al. 2023

Front. Endocrinol.

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Diabetic kidney disease (DKD) is a major microvascular complication of diabetes and a leading cause of end-stage renal disease worldwide. Autophagy plays an important role in maintaining cellular homeostasis in renal physiology. In DKD, the accumulation of advanced glycation end products induces decreased renal autophagy-related protein expression and transcription factor EB (TFEB) nuclear transfer, leading to impaired autophagy and lysosomal function and blockage of autophagic flux. This accelerates renal resident cell injury and apoptosis, mediates macrophage infiltration and phenotypic changes, ultimately leading to aggravated proteinuria and fibrosis in DKD. Natural polyphenols show promise in treating DKD by regulating autophagy and promoting nuclear transfer of TFEB and lysosomal repair. This review summarizes the characteristics of autophagy in DKD, and the potential application and mechanisms of some known natural polyphenols as autophagy regulators in DKD, with the goal of contributing to a deeper understanding of natural polyphenol mechanisms in the treatment of DKD and promoting the development of their applications. Finally, we point out the limitations of polyphenols in current DKD research and provide an outlook for their future research.

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“… 16 A study has reported that inducing Nrf2 improved HG-induced oxidative stress and activated autophagy, which contributed to protecting kidneys against the damage of hyperglycemia. 17 Kelch-like ECH-associated protein 1 (Keap1) controls the degradation of Nrf2 to restrain its transcription activity in physiological conditions. 18 The study has shown that the inactivation of Keap1 protein may activate Nrf2 pathway, thus preventing the progression of DKD.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-204-5p Ameliorates Renal Injury via Regulating Keap1/Nrf2 Pathway in Diabetic Kidney Disease

Dong,

Liu,

Bian

et al. 2024

DMSO

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Background Diabetic kidney disease (DKD) is characterized by renal fibrosis, and the pathogenesis of renal fibrosis is still not definitely confirmed. MiR-204-5p plays an important role in the regulation of fibrosis, autophagy and oxidative stress. In this study, we aimed to investigate the role of miR-204-5p on renal damage in diabetic kidneys and the underlying mechanisms involved. Methods In vivo, AAV-Ksp-miR-204-5p mimics were injected into mice via tail vein. In vitro, high glucose-induced HK-2 cells were treated with miR-204-5p inhibitor, miR-204-5p mimics, ATG5 siRNA, tertiary butyl hydroquinone (TBHQ), ML385, or 3-Methyladenine (3-MA). FISH and qRT-PCR were used to detect miR-204-5p expression. The expressions of protein and mRNA were detected by Western blotting, immunofluorescence, immunohistochemistry and qRT-PCR. The concentration of fibronectin in HK-2 cells culture medium was detected by ELISA. Results The expression of miR-204-5p in diabetic kidneys was significantly inhibited than that in control group. Delivering miR-204-5p mimics increased miR-204-5p expression, improved renal function, inhibited renal fibrosis and oxidative stress, and restored autophagy in db/db mice. In vitro, the expression of miR-204-5p was inhibited by HG treatment in HK-2 cells. MiR-204-5p mimics effectively increased miR-204-5p expression and reduced fibronectin and collagen I expression, restored autophagy dysfunction, and increased Nrf2 expression, whereas these alterations were abrogated by Nrf2 inhibitor ML385, autophagy inhibitor 3-methyladenine (3-MA, 5 mM) treatment or ATG5 siRNA transfection in HG-induced HK-2 cells. In addition, miR-204-5p inhibitor significantly inhibited miR-204-5p expression and aggravated HG-induced fibronectin and collagen I expression, autophagy dysfunction, and decreased Nrf2 expression, while these alterations were abolished by Nrf2 activator TBHQ. Furthermore, the binding of miR-204-5p with Keap1 was confirmed by luciferase reporter assay and miR-204-5p negatively regulated Keap1 expression, resulting in the activation of Nrf2 pathway. Conclusion MicroRNA-204-5p protects against the progression of diabetic renal fibrosis by restoring autophagy via regulating Keap1/Nrf2 pathway.

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Isorhapontigenin ameliorates high glucose-induced podocyte and vascular endothelial cell injuries via mitigating oxidative stress and autophagy through the AMPK/Nrf2 pathway

Cited by 9 publications

References 41 publications

Ameliorative effects of glycine on cobalt chloride‐induced hepato‐renal toxicity in rats

Ameliorative effects of glycine on cobalt chloride‐induced hepato‐renal toxicity in rats

Regulation of autophagy by natural polyphenols in the treatment of diabetic kidney disease: therapeutic potential and mechanism

MicroRNA-204-5p Ameliorates Renal Injury via Regulating Keap1/Nrf2 Pathway in Diabetic Kidney Disease

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