Emodin ameliorates renal fibrosis in rats via TGF-β1/Smad signaling pathway and function study of Smurf 2

Ma, Li; Li, Hua; Zhang, Shuchao; Xiong, Xiufang; Chen, Kean; Jiang, Peiwu; Kang, Jisoo; Deng, Gang

doi:10.1007/s11255-017-1757-x

Cited by 55 publications

(33 citation statements)

References 35 publications

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“…We used in this work the relatively novel biomarkers TGF-β1, which is used as biomarker in cardiovascular diseases (Mukherji et al 2017), and lately as a biomarker in surgery-induced renal fibrosis in rat (Ma et al 2018). Here, we found that its concentration in plasma is significantly increased in CP-induced nephrotoxicity, and that sesamin significantly ameliorated that action.…”

Section: Discussionmentioning

confidence: 87%

Ameliorative Effect of Sesamin in Cisplatin-Induced Nephrotoxicity in Rats by Suppressing Inflammation, Oxidative/Nitrosative Stress, and Cellular Damage

et al. 2020

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Nephrotoxicity of cisplatin (CP) involves renal oxidative stress and inflammation, and sesamin (a major liganin in many plants) has strong antioxidant and antiinflammatory actions. Therefore, we investigated here the possible mitigative action of sesamin on CP nephrotoxicity in rats. Sesamin was given orally (5 mg/kg/day, 10 days), and on the 7th day, some of the treated rats were injected intraperitoneally with either saline or CP (5 mg/kg). On the 11th day, rats were sacrificed, and blood and urine samples and kidneys were collected for biochemical estimation of several traditional and novel indices of renal damage in plasma and urine, several oxidative and nitrosative indices in kidneys, and assessment of histopathological renal damage. CP significantly and adversely altered all the physiological, biochemical and histopathological indices of renal function measured. Kidneys of CP‐treated rats had a moderate degree of necrosis. This was markedly lessened when CP was given simultaneously with sesamin. Sesamin treatment did not significantly alter the renal CP concentration. The results suggested that sesamin had ameliorated CP nephrotoxicity in rats by reversing the CP-induced oxidative stress and inflammation. Pending further pharmacological and toxicological studies sesamin may be considered a potentially useful nephroprotective agent.

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Section: Discussionmentioning

confidence: 87%

Ameliorative Effect of Sesamin in Cisplatin-Induced Nephrotoxicity in Rats by Suppressing Inflammation, Oxidative/Nitrosative Stress, and Cellular Damage

et al. 2020

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“…Salvia miltiorrhiza Bunge, Astragalus mongholicus Bunge, and Rheum palmatum L.) and active components (e.g. tanshinone, salvianolic acid, and emodin) reportedly possess antirenal fibrosis effect (Wang et al, 2015;Ma et al, 2017;Zhang et al, 2018). Unlike the one drug-one target concept of Western medicine, TCM emphasizes that the human body is an organic whole.…”

Section: Introductionmentioning

confidence: 99%

Deciphering the Pharmacological Mechanisms of Taohe-Chengqi Decoction Extract Against Renal Fibrosis Through Integrating Network Pharmacology and Experimental Validation In Vitro and In Vivo

Zhou

et al. 2020

Front. Pharmacol.

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“…6 Recent studies have indicated that TGF-β1 plays an important role in the progression of renal fibrosis. 7,8 In addition, Higgins et al have found that TGF-β1 signaling pathway plays a critical role during the induction of renal fibrosis. 9 Besides, it has been previously reported that activation of TGF-β1 signaling pathway can promote EMT process during the metastasis of pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

<p>Silibinin Augments the Antifibrotic Effect of Valsartan Through Inactivation of TGF-β1 Signaling in Kidney</p>

Liu

Wang

Ding

et al. 2020

DDDT

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Background: Chronic kidney disease (CKD) has become a major public health issue. Meanwhile, renal fibrosis caused by diabetic nephropathy can lead to CKD, regardless of the initial injury. It has been previously reported that silibinin or valsartan could relieve the severity of renal fibrosis. However, the effect of silibinin in combination with valsartan on renal fibrosis remains unclear. Material and Methods: Proximal tubular cells (HK-2) were treated with TGF-β1 (5 ng/mL) to mimic in vitro model of fibrosis. The proliferation of HK-2 cells was tested by CCK-8. Epithelial-mesenchymal transition (EMT) and inflammation-related gene and protein expressions in HK-2 cells were measured by qRT-PCR and Western-blot, respectively. ELISA was used to test the level of TNF-αNF-A. Additionally, HFD-induced renal fibrosis mice model was established to investigate the effect of silibinin in combination with valsartan on renal fibrosis in vivo. Results: Silibinin significantly increased the anti-fibrosis effect of valsartan in TGF-β1-treated HK-2 cells via inhibition of TGF-β1 signaling pathway. Furthermore, silibinin significantly enhanced the anti-fibrosis effect of valsartan on HFD-induced renal fibrosis in vivo through inactivation of TGF-β1 signaling pathway. Conclusion: These data indicated that silibinin markedly increased anti-fibrosis effect of valsartan in vitro and in vivo. Thus, silibinin in combination with valsartan may act as a potential novel strategy to treat renal fibrosis caused by diabetic nephropathy.

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Emodin ameliorates renal fibrosis in rats via TGF-β1/Smad signaling pathway and function study of Smurf 2

Abstract: Emodin showed an anti-fibrosis effect in surgery-induced renal fibrotic rats. And this effect was potentially achieved via down-regulating expressions of TGF-β1 and Smurf 2 and up-regulating Smad7 expression.

Cited by 55 publications

References 35 publications

Ameliorative Effect of Sesamin in Cisplatin-Induced Nephrotoxicity in Rats by Suppressing Inflammation, Oxidative/Nitrosative Stress, and Cellular Damage

Ameliorative Effect of Sesamin in Cisplatin-Induced Nephrotoxicity in Rats by Suppressing Inflammation, Oxidative/Nitrosative Stress, and Cellular Damage

Deciphering the Pharmacological Mechanisms of Taohe-Chengqi Decoction Extract Against Renal Fibrosis Through Integrating Network Pharmacology and Experimental Validation In Vitro and In Vivo

<p>Silibinin Augments the Antifibrotic Effect of Valsartan Through Inactivation of TGF-β1 Signaling in Kidney</p>

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