Beneficial effects of procyanidin B2 on adriamycin-induced nephrotic syndrome mice: the multi-action mechanism for ameliorating glomerular permselectivity injury

Zhao, Chuanping; Tang, Jingdong; Li, Xiaoya; Yan, Zihan; Zhao, Lingling; Lang, Wenbo; Yuan, Chun‐Mao; Cheng-yan, Zhou

doi:10.1039/d1fo03616e

Cited by 7 publications

(5 citation statements)

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“…[53,54] The primary mechanisms of Doxinduced kidney damage include oxidative stress, inflammation, and apoptosis. [55] Nephrotoxicity induced by Dox (at a cumulative dose of 20 mg/kg) was assessed by evaluating several parameters in serum and renal tissues. Rats receiving Dox experienced glomerular filtration disruption, which led to an increase in levels of serum urea and creatinine and a decrease in albumin; alteration in these biochemical parameters indicates the severity of the renal failure and glomerular damage, which is consistent with earlier research.…”

Section: Discussionmentioning

confidence: 99%

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Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Patel,

Yadav,

Singh

et al. 2023

J Biochem & Molecular Tox

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Doxorubicin (Dox) is an anthracycline antibiotic used to treat various cancers and shows severe toxicity in multiple organ systems, including kidneys. Evidence shows that betaine's antioxidant and anti‐inflammatory properties could prevent the onset of several disorders. Hence, the present study aims to investigate the therapeutic potential of betaine on Dox‐induced nephrotoxicity (DIN). Nephrotoxicity was induced in male Sprague Dawley rats using Dox at a dose of 4 mg/kg (cumulative dose: 20 mg/kg) by the intraperitoneal route and cotreated with betaine through oral gavage (200 and 400 mg/kg) for 28 days. At the end of the experiment, biochemical, oxidative stress parameters, histopathology, and qRT‐PCR were performed. DIN was indicated by elevated serum creatinine, urea, and decreased albumin levels representing kidney damage; the histopathological lesions (increased capsular space, renal tubule damage, and fibrosis) in renal tissues supported these biochemical findings. Interestingly, betaine treatment improves these alterations in Dox‐treated rats. Further, betaine treatment decreases the lipid peroxidation and nitrite concentration and increases the superoxide dismutases and catalase enzyme concentration in Dox‐treated rats. Fascinatingly, at the molecular level, DIN in rats shows upregulation of the Nrf2/HO‐1 gene, while betaine treatment attenuated its expression along with the downregulation of inflammatory genes (NLRP3, TLR‐4, TNF‐α, and IL‐6) and fibrosis‐related genes (TGF‐β and Acta2) expression in Dox‐treated rats. These results showed that betaine has reno‐protective properties by reducing inflammatory and fibrotic mediators and enhancing antioxidant capacity in the renal tissue of rats treated with Dox. We believe betaine can be exploited as a dietary supplement to attenuate DIN.

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Section: Discussionmentioning

confidence: 99%

“…[ 53,54 ] The primary mechanisms of Dox‐induced kidney damage include oxidative stress, inflammation, and apoptosis. [ 55 ]…”

Section: Discussionmentioning

confidence: 99%

Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Patel,

Yadav,

Singh

et al. 2023

J Biochem & Molecular Tox

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“…Recent studies have revealed the protective effects of avonoids on the kidneys. [41][42][43] In our sensitivity analysis, we did not observe evidence of the positive effects of the six subcategories of avonoids in non-obese individuals with concurrent CKD, suggesting that the contribution to survival in this group may be due to total avonoid intake. One possible explanation is a study conducted in Korea that found total avonoids in Epimedium koreanum Nakai alleviated chronic renal failure by promoting AMPK activation.…”

Section: Discussionmentioning

confidence: 99%

Investigating the Impact of Flavonoid Intake on All-Cause Mortality in Non-Obesity and Obesity with Various Complication: Insights from the National Health and Nutrition Examination Survey 2007-2010 and 2017-2018

Wang,

Xiong,

Liu

et al. 2023

Preprint

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Background: It is reported that dietary intake of flavonoid compounds can reduce all-cause mortality and mortality from specific vascular diseases and cancers, but whether dietary intake of flavonoid can affect obesity and obesity-related comorbidities is unknown. Aim: The main objective is to investigate the relationship between flavonoid intake and all-cause mortality in both obese and non-obese individuals, and in combination with diabetes, non-alcoholic fatty liver disease (NAFLD), cardiovascular disease (CVD), and chronic kidney disease (CKD). Methods: This study included NHANES participants from 2007-2010 and 2017-2018. Cox regression analysis evaluated the impact of total flavonoid intake on all-cause mortality among participants with varying comorbidity profiles. Subgroup analysis was conducted by separately analyzing the six sub-classes of total flavonoids (anthocyanidins, flavan-3-ols, flavanones, flavones, flavonols, and isoflavones). Sensitivity analysis investigated the impact of total flavonoid intake on all-cause mortality among patients with different comorbidities. Results: During a median follow-up period of 9.92 years (interquartile range (IQR), 5.54-14.29 years), a total of 639 participants died. In comparison to non-obese participants, cox regression analysis revealed a favorable impact of flavonoid intake on all-cause mortality in obese participants with CKD (hazard ratio (HR): 0.22, 95% CI: 0.11-0.44), metabolically healthy obese (MHO) participants (HR: 0.15, 95% CI: 0.07-0.35), obese individuals with diabetes (HR: 0.51, 95% CI: 0.29-0.88), and obese individuals with comorbid CVD (HR: 0.37, 95% CI: 0.17-0.83). Restricted cubic spline (RCS) analysis indicated a non-linear relationship in obese participants, with optimal intake levels ranging from 319.4978 to 448.6907 mg/day. Subgroup analysis revealed varying effects of total flavonoid components in different health conditions, with hazard ratios ranging from 0.06 for higher levels of flavonol to 0.59 for higher levels of anthocyanidins. Conclusions: In comparison to unhealthy individuals without obesity, those with unhealthy obesity who consume flavonoids show a reduced risk of all-cause mortality.

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“…A transmission electron microscope (TEM; HT7800; Hitachi, Japan) was used to evaluate ultrastructural changes in the kidney. The protocol of TEM analysis is in accordance with our prior reports …”

Section: Methodsmentioning

confidence: 99%

“…The protocol of TEM analysis is in accordance with our prior reports. 36 2.6. Prussian Blue Staining.…”

Section: Histopathological Analysis and Ultrastructuralmentioning

confidence: 99%

“Multiomics” Analyses Combined with Systems Pharmacology Reveal the Renoprotection of Mangiferin Monosodium Salt in Rats with Diabetic Nephropathy: Focus on Improvements in Renal Ferroptosis, Renal Inflammation, and Podocyte Insulin Resistance

Zhao

Gao

et al. 2022

J. Agric. Food Chem.

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We explored the protection of mangiferin monosodium salt (MGM) on kidney injury in rats with streptozotocin (STZ)-induced diabetic nephropathy (DN) by “multiomics” analysis combined with systems pharmacology, with a specific focus on ferroptosis, inflammation, and podocyte insulin resistance (IR) signaling events in kidneys. MGM treatment afforded renoprotective effects on rats with STZ-induced DN by alleviating systemic IR-induced renal inflammation and podocyte IR. These mechanisms were correlated mainly with the MGM treatment-induced inhibition of the mitogen-activated protein kinase/nuclear factor-kappa B axis and activation of the phosphorylated insulin receptor substrate 1(Tyr608)/phosphorylated phosphatidylinositol 3-kinase/phosphorylated protein kinase B axis in the kidneys of DN rats. MGM had an ameliorative function in renal ferroptosis in rats with STZ-induced DN by upregulating mevalonate-mediated antioxidant capacities (glutathione peroxidase 4 and ferroptosis suppressor protein 1/coenzyme Q10 axis) and weakening acyl-CoA synthetase long-chain family member 4-mediated proferroptotic generation of lipid drivers in kidneys. MGM may be a promising alternative strategy for the treatment of DN.

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Beneficial effects of procyanidin B2 on adriamycin-induced nephrotic syndrome mice: the multi-action mechanism for ameliorating glomerular permselectivity injury

Abstract: Despite considerable advances in prevention, diagnosis, and therapy, nephrotic syndrome (NS) remains a significant cause of high morbidity and mortality globally. As a result, there is an urgent need to...

Cited by 7 publications

References 162 publications

Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Betaine alleviates doxorubicin‐induced nephrotoxicity by preventing oxidative insults, inflammation, and fibrosis through the modulation of Nrf2/HO−1/NLRP3 and TGF‐β expression

Investigating the Impact of Flavonoid Intake on All-Cause Mortality in Non-Obesity and Obesity with Various Complication: Insights from the National Health and Nutrition Examination Survey 2007-2010 and 2017-2018

“Multiomics” Analyses Combined with Systems Pharmacology Reveal the Renoprotection of Mangiferin Monosodium Salt in Rats with Diabetic Nephropathy: Focus on Improvements in Renal Ferroptosis, Renal Inflammation, and Podocyte Insulin Resistance

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