Shen-Kang protects against tacrolimus-induced renal injury

Korean J Intern Med. 2019 Sep;34(5):1078-1090. doi: 10.3904/kjim.2017.276. Epub 2018 Feb 12.

Abstract

Background/aims: Evidence 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.

Methods: Rats 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.

Results: Administration 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).

Conclusion: SK protects against TAC-induced renal injury.

Keywords: Apoptosis; Oxidative stress; Shen-Kang; Tacrolimus; Transforming growth factor beta1.

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis Regulatory Proteins / metabolism
  • Cytokines / metabolism
  • Cytoprotection
  • Disease Models, Animal
  • Drugs, Chinese Herbal / pharmacology*
  • Extracellular Matrix Proteins / metabolism
  • Kidney / drug effects*
  • Kidney / metabolism
  • Kidney / pathology
  • Kidney Diseases / chemically induced
  • Kidney Diseases / metabolism
  • Kidney Diseases / pathology
  • Kidney Diseases / prevention & control*
  • Male
  • Oxidative Stress / drug effects
  • Protective Agents / pharmacology*
  • Rats, Sprague-Dawley
  • Signal Transduction
  • Tacrolimus*
  • Transforming Growth Factor beta / metabolism
  • Transforming Growth Factor beta1 / metabolism

Substances

  • Apoptosis Regulatory Proteins
  • Cytokines
  • Drugs, Chinese Herbal
  • Extracellular Matrix Proteins
  • Protective Agents
  • Tgfb1 protein, rat
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • shenkang
  • betaIG-H3 protein
  • Tacrolimus