Kidney protection effects of dihydroquercetin on diabetic nephropathy through suppressing ROS and NLRP3 inflammasome

Ding, Tao; Wang, Shaofei; Zhang, Xu-Yao; Zai, Wenjing; Fan, Jiajun; Chen, Wei; Bian, Qian; Luan, Jingyun; Shen, Yilan; Zhang, Yanda; Ju, Dianwen; Mei, Xiaobin

doi:10.1016/j.phymed.2018.01.026

Cited by 114 publications

(73 citation statements)

References 25 publications

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“…An additional biomolecule called taxifolin (or dihydroquercetin (DHQ)) might have a promising effect on DN. Recent work showed that DHQ has protective kidney properties similar to losartan (angiotensin II inhibitor) including attenuating albuminuria, hyperglycemia, and lipid metabolism disorders, and modifying renal lesions in DN possibly by suppressing ROS and NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) inflammasome [210]. Another study found that DHQ attenuates DN in STZ diabetic rats; CAV1 and p-NFκB expression was reduced upon DHQ administration, which suggests that DHQ might have its beneficial effects on DN by downregulating CAV1 [211].…”

Section: Future Perspectivesmentioning

confidence: 99%

Role of Caveolin-1 in Diabetes and Its Complications

Haddad

Madhoun

Nizam

et al. 2020

Oxidative Medicine and Cellular Longevity

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It is estimated that in 2017 there were 451 million people with diabetes worldwide. These figures are expected to increase to 693 million by 2045; thus, innovative preventative programs and treatments are a necessity to fight this escalating pandemic disorder. Caveolin-1 (CAV1), an integral membrane protein, is the principal component of caveolae in membranes and is involved in multiple cellular functions such as endocytosis, cholesterol homeostasis, signal transduction, and mechanoprotection. Previous studies demonstrated that CAV1 is critical for insulin receptor-mediated signaling, insulin secretion, and potentially the development of insulin resistance. Here, we summarize the recent progress on the role of CAV1 in diabetes and diabetic complications.

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Section: Future Perspectivesmentioning

confidence: 99%

Role of Caveolin-1 in Diabetes and Its Complications

Haddad

Madhoun

Nizam

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…As a potential therapeutic agents against inflammation and DN, Compound K can inhibit the TXNIP/NLRP3 signal pathway and ameliorate the insulin resistance to protect the tubular inflammation (Chen et al, 2016c). Dihydroquercetin also shows a protective role in DN by suppressing the ROS and the NLRP3 inflammasome (Ding et al, 2018). However, further research is required to find and validate effective drugs concerning the role of NLRP3 inflammasome.…”

Section: Inflammasomes In Diabetic Nephropathymentioning

confidence: 99%

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

Xiang

Zhu

et al. 2020

Front. Cell Dev. Biol.

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Inflammasomes, multiprotein complex induced by harmful factors in the body, play a crucial role in innate immunity. Activation of inflammasomes lead to the activation of casepase-1 and then the secretion of inflammatory cytokines, including IL-1β and IL-18, subsequently leading to a type of cell death called pyroptosis. There are two types of signaling pathways involved in the process of inflammasome activation: the canonical and the non-canonical signaling pathway. The canonical signaling pathway is mainly dependent on casepase-1; the non-canonical signal pathway, which was recently discovered, is mainly dependent on caspase-11, but is also meditated by caspase-4, caspase-5, and caspase-8. Kidney inflammation is basically associated with inflammatory factor exudation and inflammatory cell infiltration. Several studies have showed that inflammasomes are closely related to kidney diseases, especially the NOD-, LRR-and pyrin domain-containing 3 (NLRP3) inflammasome, which play a role in regulating kidney inflammation and fibrosis. In this review, we focus on the relationship between inflammasomes and kidney diseases, especially the role of the NLRP3 inflammasome in different kinds of kidney disease via both canonical and non-canonical signal pathways.

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“…Several inducers of NLRP3 activation have been previously identified (Abais, et al, 2015;Ding et al, 2018), but the inhibitiors of NLRP3 was rarely reported. Autophagy is involved in the removal of degraded proteins, damaged organelles, and other cytoplasmic constituents, and has been implicated in the inhibition of NLRP3 expression recently (Xu et al, 2018;Zhong et al, 2016a).…”

Section: Introductionmentioning

confidence: 99%

Astragaloside IV protects against cisplatin-induced liver and kidney injury via autophagy-mediated inhibition of NLRP3 in rats

Gao

Tao

et al. 2019

J. Toxicol. Sci.

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The aim of this study was to explore the role of the NOD-like receptor family, pyrin domain containing (NLRP3) inflammasome and autophagy in Astragaloside IV (AS IV)-mediated protection against cisplatin-induced liver and kidney injury in rats. Rats were intraperitoneally administered cisplatin at a dose of 15 mg/kg and orally administered AS IV for 7 days. Histopathological and biochemical analysis were used to assess liver and kidney function. The levels and localization of NLRP3 and autophagy-associated protein were determined by Western blot and immunohistochemistry. Intraperitoneal administration of cisplatin induced acute liver and kidney injury, and activated the NLRP3 inflammasome. Oral administration of AS IV for 7 days protected against the cisplatin-induced injury, and inhibited the expression of NLRP3, as well as the production of pro-inflammatory cytokines. Moreover, cisplatin modulated the conversion of LC3 II and the expression of p62, thereby inhibiting autophagy and the activation of NLRP3. AS IV effectively protected against cisplatin-induced injury by inducing autophagy and limiting the expression of NLRP3. Autophagy-mediated NLRP3 inhibition might play a crucial role in AS IV-mediated protection against cisplatin-induced toxicity. These results provide evidence of a novel therapeutic that may be used to alleviate the toxic effects of platinum-based chemotherapy.

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Kidney protection effects of dihydroquercetin on diabetic nephropathy through suppressing ROS and NLRP3 inflammasome

Cited by 114 publications

References 25 publications

Role of Caveolin-1 in Diabetes and Its Complications

Role of Caveolin-1 in Diabetes and Its Complications

Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways

Astragaloside IV protects against cisplatin-induced liver and kidney injury via autophagy-mediated inhibition of NLRP3 in rats

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