ArticleThe Korean journal of internal medicine2019
Shen-Kang protects against tacrolimus-induced renal injury.
Article in The Korean journal of internal medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Efficacy and safety of activating blood circulation and removing blood stasis of Traditional Chinese Medicine for managing renal fibrosis in patients with chronic kidney disease: a systematic review and Meta-analysis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Pooled it
- Chinese herbal medicine alleviates renal impairment induced by immunosuppressants in patients post living donor liver transplantation.Journal of traditional and complementary medicine · 2025Article
- Pathogenesis and management of renal fibrosis induced by unilateral ureteral obstruction.Kidney research and clinical practice · 2024Article
- Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death.The Korean journal of internal medicine · 2021Article
- Exogenous pancreatic kininogenase protects against renal fibrosis in rat model of unilateral ureteral obstruction.Acta pharmacologica Sinica · 2020Article
- Renoprotective Effects of Alpha-1 Antitrypsin against Tacrolimus-Induced Renal Injury.International journal of molecular sciences · 2020Article
- The therapeutic efficacy of water-soluble coenzyme Q10 in an experimental model of tacrolimus-induced diabetes mellitus.The Korean journal of internal medicine · 2020Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
aimsEvidence suggests that Shen-Kang (SK), a traditional Chinese herbal medicine, protects against various types of renal injury. In this study, we evaluated whether SK treatment confers renoprotection in a rat model of chronic tacrolimus (TAC) nephropathy.
methodsRats were treated daily with TAC (1.5mg/kg, subcutaneously) and SK (450 mg/kg, intravenously) for 4 weeks. The effects of SK on TAC-induced renal injury were assessed by measuring renal function, urine albumin excretion, histopathology, inflammatory cell infiltration, expression of profibrotic (transforming growth factor β1 [TGF-β1] and TGF-β inducible gene-h3 [βig-h3]) and proinflammatory cytokines, oxidative stress, and apoptotic cell death.
resultsAdministration of SK preserved glomerular integrity (fractional mesangial area and Wilms tumor 1-positive glomeruli), attenuated tubulointerstitial fibrosis, and reduced the number of ectodermal dysplasia 1-positive cells, and this was paralleled by improved urine albumin excretion and renal dysfunction. At the molecular level, SK treatment suppressed expression of TGF-β1/Smad2/3, βig-h3, and proinflammatory cytokines. Oxidative stress and apoptotic cell death were significantly decreased with SK treatment, and apoptosis-related genes were regulated toward cell survival (active caspase-3 and the B-cell lymphoma-2/Bcl2-associated X [Bcl-2/Bax] ratio).
conclusionSK protects against TAC-induced renal injury.
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