Berberine ameliorates renal interstitial fibrosis induced by unilateral ureteral obstruction in rats

Wang, Fang‐Ming; Yang, Yujie; Ma, Lulin; Tian, Xiaojun; He, Yaqiang

doi:10.1111/nep.12271

Cited by 29 publications

(15 citation statements)

References 28 publications

(52 reference statements)

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“…Poricoic acid G and poricoic acid H suppressed TGF-β/Smad pathway by selectively inhibiting the phosphorylation of Smad3 via blocking the interactions of SARA with TGFβRI and Smad3 [178]. Similarly, renal fibrosis in a variety of animal models were attenuated or suppressed through TGF-β/Smads and NF-κB-mediated pathways by administration of compounds isolated from various natural products, such as GQ5 [179], arctigenin [98], curcumin [180,181], resveratrol [182], berberine [183,184], sinomenine [185], rutin [186], oxymatrine [149,187], bergenin [188], oleanolic acid [189], tanshinone IIA [190], leonurine [191]; (+/−)-sinensilactam A [192], epigallocatechin-3-gallate [193] and astragaloside IV [194,195].…”

Section: Specific Inhibition Of Smads Signaling By Natural Productsmentioning

confidence: 99%

Central role of dysregulation of TGF-β/Smad in CKD progression and potential targets of its treatment

Chen

Yang

et al. 2018

Biomedicine & Pharmacotherapy

267

200

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Chronic kidney disease (CKD) has emerged as a major cause of morbidity and mortality worldwide. Interstitial fibrosis, glomerulosclerosis and inflammation play the central role in the pathogenesis and progression of CKD to end stage renal disease (ESRD). Transforming growth factor-β1 (TGF-β1) is the central mediator of renal fibrosis and numerous studies have focused on inhibition of TGF-β1 and its downstream targets for treatment of kidney disease. However, blockade of TGF-β1 has not been effective in the treatment of CKD patients. This may be, in part due to anti-inflammatory effect of TGF-β1. The Smad signaling system plays a central role in regulation of TGF-β1 and TGF-β/Smad pathway plays a key role in progressive renal injury and inflammation. This review provides an overview of the role of TGF-β/Smad signaling pathway in the pathogenesis of renal fibrosis and inflammation and an effective target of anti-fibrotic therapies. Under pathological conditions, Smad2 and Smad3 expression are upregulated, while Smad7 is downregulated. In addition to TGF-β1, other pathogenic mediators such as angiotensin II and lipopolysaccharide activate Smad signaling through both TGF-β-dependent and independent pathways. Smads also interact with other pathways including nuclear factor kappa B (NF-κB) to regulate renal inflammation and fibrosis. In the context of renal fibrosis and inflammation, Smad3 exerts profibrotic effect, whereas Smad2 and Smad7 play renal protective roles. Smad4 performs its dual functions by transcriptionally promoting Smad3-dependent renal fibrosis but simultaneously suppressing NF-κB-mediated renal inflammation via Smad7-dependent mechanism. Furthermore, TGF-β1 induces Smad3 expression to regulate microRNAs and Smad ubiquitination regulatory factor (Smurf) to exert its pro-fibrotic effect. In conclusion, TGF-β/Smad signaling is an important pathway that mediates renal fibrosis and inflammation. Thus, an effective anti-fibrotic therapy via inhibition of Smad3 and upregulation of Smad7 signaling constitutes an attractive approach for treatment of CKD.

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Section: Specific Inhibition Of Smads Signaling By Natural Productsmentioning

confidence: 99%

Central role of dysregulation of TGF-β/Smad in CKD progression and potential targets of its treatment

Chen

Yang

et al. 2018

Biomedicine & Pharmacotherapy

267

200

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“…It is an antimicrobial drug routinely prescribed for the treatment of diarrhea in various Asian countries ( 11 ). In addition to this well-known and widely recognized effect, it has been demonstrated that BBR also regulates the activity of transcription factors essential for the inflammatory response ( 12 ). BBR has been shown to provide intestinal and cerebral protection against I/R-induced injury ( 13 , 14 ); however, the effects of BBR against myocardial I/R injury are yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Berberine attenuates myocardial ischemia reperfusion injury by suppressing the activation of PI3K/AKT signaling

Zhu

2016

Experimental and Therapeutic Medicine

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Berberine (BBR), an isoquinoline alkaloid originally isolated from the Chinese herb Coptis chinensis (Huanglian), exhibits anti-inflammatory and immunosuppressive properties. Since myocardial ischemia/reperfusion (I/R) injury is associated with an excessive immune response, the current study was conducted to investigate the impact of BBR on myocardial I/R injury, a common disorder in clinical settings. Preconditioning of Sprague-Dawley rats with BBR (100 mg/kg/day, by gavage) for 14 days prior to the induction of I/R significantly attenuated myocardial I/R injury as manifested by a reduction in the incidence of ventricular arrhythmia and the amelioration of myocardial histological changes. These effects were found to be associated with the suppression of the phosphoinositide 3-kinase/AKT signaling pathway and the subsequent reduction of the expression of interleukin (IL)-6, IL-1β, and tumor necrosis factor-α in the serum and myocardial tissue. These results indicate that BBR has the potential be an effective alternative therapy for the prevention and treatment of myocardial I/R injury in clinical practice.

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“…15 Similarly, another rodent model also described that berberine treatment improves renal interstitial fibrosis of obstructed kidney. 16 In addition, it has also been documented that berberine ameliorates hypertension-induced renal damage in spontaneous hypertensive rats. 17 However, the effect of berberine in association with GM-induced nephrotoxicity has been not explored.…”

Section: Introductionmentioning

confidence: 99%

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

et al. 2016

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Background: Gentamicin (GM) is the commonly used antibiotics against Gram-negative infection, but the nephrotoxic potential of drug limit its clinical interest. The aim of this study was to investigate the protective effect of berberine (BER) against GM-induced nephrotoxicity and possible underlying mechanisms. Material and methods: The rats were divided into various group, namely normal, GM-control, GM þ BER (10, 20, and 40 mg/kg). Nephrotoxicity was induced by intraperitoneal administration of GM (120 mg/kg) for 7 consecutive days. BER (10, 20, and 40 mg/kg; p.o.) was also administered for the 7 days. Various biochemical, molecular, and histological parameters were assessed in serum and kidney. Results: GM-administration significantly increased (p < 0.001) the serum creatinine and blood urea nitrogen (BUN) as well as renal malonaldehyde (MDA), nitric oxide (NO) along with Kidney Injury Molecule-1 (KIM-1), Neutrophil gelatinase-associated lipocalin (NGAL), and nuclear factor-kappa B (NF-KB) renal mRNA expressions. In addition, GM also significantly decreased (p < 0.001) the renal superoxide dismutase (SOD), reduced glutathione (GSH), B-cell lymphoma 2 (Bcl-2) mRNA expression, and mitochondrial enzymes (NADH dehydrogenase and cytochrome c oxidase) activities. Rats treated with BER (20 and 40 mg/kg; p.o.) significantly and dose-dependently (p < 0.05 and p < 0.01) restore the altered levels of antioxidant, inflammatory, apoptosis, AKI markers as well as depleted mitochondrial enzymes. Histopathological abbreviations were also ameliorated by BER administration. Conclusion: Berberine exerts renoprotective effects through its anti-oxidant, anti-inflammatory, and anti-apoptotic properties.

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Berberine ameliorates renal interstitial fibrosis induced by unilateral ureteral obstruction in rats

Abstract: Berberine treatment ameliorates RIF in a UUO rat model by inhibition of oxidative stress, inflammatory responses, and TGF-β1/pSmad3 signalling.

Cited by 29 publications

References 28 publications

Central role of dysregulation of TGF-β/Smad in CKD progression and potential targets of its treatment

Central role of dysregulation of TGF-β/Smad in CKD progression and potential targets of its treatment

Berberine attenuates myocardial ischemia reperfusion injury by suppressing the activation of PI3K/AKT signaling

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

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