Protective effect of isoliquiritigenin on experimental diabetic nephropathy in rats: Impact on Sirt-1/NFκB balance and NLRP3 expression

Alzahrani, Sharifa; Zaitone, Sawsan A.; Said, Eman; El‐Sherbiny, Mohamed; Ajwah, Sadeem M.; Alsharif, Sumayyah Yasser; Elsherbiny, Nehal M.

doi:10.1016/j.intimp.2020.106813

Cited by 44 publications

(15 citation statements)

References 69 publications

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“…Interestingly, accumulating studies have shown that TMAO accelerates the progression of many inflammatory diseases, including cardiovascular disease, CKD, and central nervous system disease, by activating inflammatory pathways, such as the MAPK, NF-κB, and NLRP3 signaling pathways, and then increasing pro-inflammatory molecules, including tumor necrosis factor alpha, IL-6, IL-1β, and IL-18 ( Seldin et al, 2016 ; Sun et al, 2017 ; Geng et al, 2018 ; Zhang et al, 2019 , 2020 ). The NLRP3 inflammasome, which comprises different domains, such as NLRP3, ASC, caspase-1, IL-1β, and IL-18, has been shown to have a crucial role in DKD ( Ram et al, 2020 ), and to be related to renal inflammation and fibrosis ( Alzahrani et al, 2020 ; An et al, 2020 ). One study has shown that NLRP3 knockout in diabetic mice protects against diabetic nephropathy, improves the urine albumin/creatinine ratio, and attenuates glomerular hypertrophy, mesangial expansion, interstitial fibrosis, inflammation, and TGF-β 1 expression ( Wu et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Trimethylamine N-Oxide Exacerbates Renal Inflammation and Fibrosis in Rats With Diabetic Kidney Disease

et al. 2021

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The gut microbiota plays a pivotal role in the onset and development of diabetes and its complications. Trimethylamine N-oxide (TMAO), a gut microbiota-dependent metabolite of certain nutrients, is associated with type 2 diabetes and its complications. Diabetic kidney disease (DKD) is one of the most serious microvascular complications. However, whether TMAO accelerates the development of DKD remains unclear. We tested the hypothesis that TMAO accelerates the development of DKD. A high-fat diet/low-dose streptozotocin-induced diabetes rat model was established, with or without TMAO in the rats’ drinking water. Compared to the normal rats, the DKD rats showed significantly higher plasma TMAO levels at the end of the study. TMAO treatment not only exacerbated the kidney dysfunction of the DKD rats, but also renal fibrosis. Furthermore, TMAO treatment activated the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome and resulted in the release of interleukin (IL)-1β and IL-18 to accelerate renal inflammation. These results suggested that TMAO aggravated renal inflammation and fibrosis in the DKD rats, which provides a new perspective to understand the pathogenesis of DKD and a potential novel target for preventing the progression of DKD.

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Section: Discussionmentioning

confidence: 99%

Trimethylamine N-Oxide Exacerbates Renal Inflammation and Fibrosis in Rats With Diabetic Kidney Disease

et al. 2021

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“…The role of SIRT1 in kidney diseases has been focused in recent years. In streptozotocin (STZ)-induced diabetic rats, increased oxidative stress and decreased SIRT1 expression were observed in the kidneys [45]. And the enhancement of SIRT1 activity was indicated to alleviate the kidney inflammation injury and oxidative damage [46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

Ye¹,

Yang²,

Liu³

et al. 2021

Int. J. Biol. Sci.

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Renal tubular cell injury induced by calcium oxalate (CaOx) is a critical initial stage of kidney stone formation. Theaflavin (TF) has been known for its strong antioxidative capacity; however, the effect and molecular mechanism of TF against oxidative stress and injury caused by CaOx crystal exposure in kidneys remains unknown. To explore the potential function of TF on renal crystal deposition and its underlying mechanisms, experiments were conducted using a CaOx nephrocalcinosis mouse model established by glyoxylate intraperitoneal injection, and HK-2 cells were subjected to calcium oxalate monohydrate (COM) crystals, with or without the treatment of TF. We discovered that TF treatment remarkably protected against CaOx-induced kidney oxidative stress injury and reduced crystal deposition. Additionally, miR-128-3p expression was decreased and negatively correlated with SIRT1 level in mouse CaOx nephrocalcinosis model following TF treatment. Moreover, TF suppressed miR-128-3p expression and further abolished its inhibition on SIRT1 to attenuate oxidative stress in vitro. Mechanistically, TF interacted with miR-128-3p and suppressed its expression. In addition, miR-128-3p inhibited SIRT1 expression by directly binding its 3'-untranslated region (UTR). Furthermore, miR-128-3p activation partially reversed the acceerative effect of TF on SIRT1 expression. Taken together, TF exhibits a strong nephroprotective ability to suppress CaOx-induced kidney damage through the recovery of the antioxidant defense system regulated by miR-128-3p/SIRT1 axis. These findings provide novel insights for the prevention and treatment of renal calculus.

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“…We recorded the area, area fraction, limit to threshold, and display label (Analyze → Measure). Two different sections from each animal were analyzed, and from each section, (6-10) different non-overlapping fields were examined (12-20 fields/animal) [26].…”

Section: Histopathological Examinationmentioning

confidence: 99%

α-Lipoic Acid Protects against Cyclosporine A-Induced Hepatic Toxicity in Rats: Effect on Oxidative Stress, Inflammation, and Apoptosis

El-Mancy

Elsherbini

Al-Serwi

et al. 2022

Toxics

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The clinical application of cyclosporine A (CsA) as an immunosuppressive agent is limited by its organ toxicity. We aimed to evaluate the effectiveness of α-lipoic acid against CsA-induced hepatotoxicity and to delineate the underlying molecular mechanisms. Male Wistar rats (n = 24, 8 per each group) received the vehicle, CsA (25 mg/kg) and/or ALA (100 mg/kg, p.o.) for 3 weeks. Biochemical markers of liver function (serum ALT, AST, ALP < GGT), oxidative stress (MDA, TAC, SOD, GSH, Nrf2/HO-1), inflammation (NF-κB, CD68, iNOS, NO, COX-2), and apoptosis (caspase-3) were assessed in serum and tissue. Liver histological analysis using H&E and Sirius red was performed. The development of liver injury in CsA-treated animals was indicated by elevated levels of liver enzymes, oxidants/antioxidants imbalance, inflammatory cells infiltration, up-regulated expression of inflammatory mediators, and apoptosis. These changes were associated with altered architecture of hepatic cells and fibrous connective tissue. ALA co-administration protected against CsA-induced liver damage and ameliorated biochemical changes and cellular injury. In conclusion, ALA demonstrated hepatoprotective potential against CsA-induced liver injury through combating oxidative stress, inflammation, and apoptosis, highlighting ALA as a valuable adjunct to CsA therapy.

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Protective effect of isoliquiritigenin on experimental diabetic nephropathy in rats: Impact on Sirt-1/NFκB balance and NLRP3 expression

Cited by 44 publications

References 69 publications

Trimethylamine N-Oxide Exacerbates Renal Inflammation and Fibrosis in Rats With Diabetic Kidney Disease

Trimethylamine N-Oxide Exacerbates Renal Inflammation and Fibrosis in Rats With Diabetic Kidney Disease

Theaflavin protects against oxalate calcium-induced kidney oxidative stress injury via upregulation of SIRT1

α-Lipoic Acid Protects against Cyclosporine A-Induced Hepatic Toxicity in Rats: Effect on Oxidative Stress, Inflammation, and Apoptosis

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