Protective effect of baicalein on renal ischemia/reperfusion injury in the rat

Wu, Kefei; Li, Hongyan; Tian, Jianwei; Lei, Weimin

doi:10.3109/0886022x.2014.991999

Cited by 16 publications

(15 citation statements)

References 19 publications

(26 reference statements)

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“…Furthermore, baicalein reduces airway inflammation in allergen and IL-1b-induced asthma model. Baicalein also exhibits protective properties in kidney injury (Wu et al 2014) and fibrosis (Wang et al 2012). It promotes the recovery of renal function, alleviates kidney injury in ischemia-reperfusion (I/R) model, and ameliorates kidney fibrosis through downregulated TGF-b1 and Smad-2 in UUO mice model.…”

Section: Introductionmentioning

confidence: 97%

Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways

Wang

Zhou

et al. 2015

J Mol Hist

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Baicalein is a natural flavonoid that possesses notable anti-inflammatory effects. In this study, we detected whether baicalein protects against inflammatory response in unilateral ureteral obstruction mice model to ameliorate tubulointerstitial fibrosis. Baicalein treatment significantly attenuated tubulointerstitial fibrosis by markedly reducing fibronectin and collagen-I. The downregulation of alpha-smooth muscle actin and upregulation of E-cadherin indicated that the epithelial-mesenchymal transition process was suppressed. Furthermore, baicalein administration blocked the infiltration of macrophages and lymphocytes, as evidenced by the significantly reduced CD68 and CD3 positive cells. Meanwhile, the mRNA expression of the pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and monocyte chemotactic protein in baicalein-treated groups was markedly reduced compared with the vehicle-treated group. More importantly, unilateral ureteral obstruction induced the activation of NF-κB and mitogen-activated protein kinase signal pathways to switch on inflammatory response to aggravate kidney fibrosis, but these effects were mitigated by baicalein. These data demonstrate that baicalein could inhibit inflammatory process via inactivation of NF-κB and MAPK signal pathways to execute its anti-fibrotic actions in obstructive kidney disease.

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Section: Introductionmentioning

confidence: 97%

Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways

Wang

Zhou

et al. 2015

J Mol Hist

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“…Erythropoietin pretreatment ameliorates renal IRI by activating PI3K/Akt signaling and inhibiting tubulointerstitial inflammation [23,24]. By anti-inflammatory effects and by reducing oxidative stress, atorvastatin, baicalein and mangiferin reduce renal IRI [25][26][27][28]. Preconditioning with triiodothyronine and gabexate is also reported to ameliorate renal IRI in rats [29][30][31].…”

Section: Introductionmentioning

confidence: 99%

Propofol Prevents Renal Ischemia-Reperfusion Injury via Inhibiting the Oxidative Stress Pathways

Zhong

Lei

et al. 2015

Cell Physiol Biochem

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Background/Aims: Renal ischemia/reperfusion injury (IRI) is a risk for acute renal failure and delayed graft function in renal transplantation and cardiac surgery. The purpose of this study is to determine whether propofol could attenuate renal IRI and explore related mechanism. Methods: Male rat right kidney was removed, left kidney was subjected to IRI. Propofol was intravenously injected into rats before ischemia. The kidney morphology and renal function were analyzed. The expression of Bax, Bcl-2, caspase-3, cl-caspase-3, GRP78, CHOP and caspase-12 were detected by Western blot analysis. Results: IR rats with propofol pretreatment had better renal function and less tubular apoptosis than untreated IR rats. Propofol pretreated IR rats had lower Bax/Bcl-2 ratio and less cleaved caspase-3. The protein expression levels of GRP78, CHOP and caspase-12 decreased significantly in propofol pretreated IR rats. In vitro cell model showed that propofol significantly increased the viability of NRK-52E cells that were subjected to hypoxia/reoxygenation (H/R) in a dose-dependent manner. The effect of propofol on the expression regulation of Bax, Bcl-2, caspase-3, GRP78, CHOP was consistent in both in vitro and in vivo models. Conclusion: Experimental results suggest that propofol prevents renal IRI via inhibiting oxidative stress.

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“…This compound has been shown to possess a variety of biological characteristics, including antioxidative 16 and anti-inflammatory effects, 17 tumour growth inhibition 18 and protection of ischaemia/reperfusion injury. 19 It has been proven to attenuate fibrotic activities in cardiac fibroblasts via mitogen-activated protein kinase signalling 20 and to suppress hepatic stellate cell migration by inhibiting monocyte chemoattractant protein-1 expression. 21 However, the effect of baicalein on human dermal fibroblasts (normal or exuberant) and the potential molecular mechanisms of baicalein are still unknown.…”

mentioning

confidence: 99%

Baicalein attenuates hypertrophic scar formation via inhibition of the transforming growth factor‐β/Smad2/3 signalling pathway

et al. 2015

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Protective effect of baicalein on renal ischemia/reperfusion injury in the rat

Cited by 16 publications

References 19 publications

Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways

Baicalein attenuates renal fibrosis by inhibiting inflammation via down-regulating NF-κB and MAPK signal pathways

Propofol Prevents Renal Ischemia-Reperfusion Injury via Inhibiting the Oxidative Stress Pathways

Baicalein attenuates hypertrophic scar formation via inhibition of the transforming growth factor‐β/Smad2/3 signalling pathway

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