TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000520810
  • Gene Name:IKBKB
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:NF-KB signaling pathway
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB01065
  • Drug Name:Melatonin
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:diabetic nephropathy
  • Tissue:tissues

Other information

  • Title:Melatonin Ameliorates Renal Fibrosis Through the Inhibition of NF-κB and TGF-β1/Smad3 Pathways in db/db Diabetic Mice
  • Journal:Archives of Medical Research
  • Published:2020
  • PubMed ID:32473749
  • Abstract:Objective:To investigate the effects and molecular mechanism of melatonin (MT) on NF-κB and TGF-β/Smad3 signaling pathways in db/db diabetic mice. Methods:db/db diabetic mice were divided into five groups treated with melatonin at doses of 50, 100, 200 μg/kg, the urinary concentration was detected by ELISA, renal histology was observed in PAS paining. Mouse mesangial cells were divided into mannitol control group, normal control group, normal control + MT group, high glucose group, high glucose + different concentrations (10, 100, 1000) μmol/L MT group. The proliferation of mesangial cells was detected by EdU kit; the expression of NF-κBp65, ColⅣ and Fn were detected by laser confocal system; the concentrations and mRNA levels of ColⅣ and Fn were detected by ELISA and qRT-PCR. the expressions of ColⅣ, Fn, IκB, p-IκB, TGF-β1, Smad3 and p-Smad3 were detected by Western blot in renal tissues and mesangial cells. Results:MT treatment could markedly improve the kidney histopathologic lesions. Compared with the db/m mice, 24 h urinary albumin excretion rate (UAER) and the expressions of ColIV, Fn, p-IκB/IκB, NF-κBp65, TGF-β1 and p-Smad3/Smad3 were decreased after melatonin treatment (p <0.05). Compared with the control group, the proliferation function of mesangial cells in high glucose group was significantly enhanced, and the expressions of ColIV, Fn, p-IκB/IκB, NF-κBp65, TGF-β1 and p-Smad3/Smad3 in mesangial cells were significantly up-regulated (p <0.05), and these changes were significantly lowered in MT treatment. Conclusion:Melatonin can inhibit renal inflammation and fibrosis by inhibiting the NF-κB and TGF-β1/Smad3 signaling pathways, and melatonin may be a promising therapeutic target in diabetic nephropathy.
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