title: Baicalin ameliorates renal fibrosis via inhibition of transforming growth factor β1 production and downstream signal transduction.
abstract: Previous studies have demonstrated the potential antifibrotic effects of baicalin in vitro, via examination of 21 compounds isolated from plants. However, its biological activity and underlying mechanisms of action in vivo remain to be elucidated. The present study aimed to evaluate the effect of baicalin on renal fibrosis in vivo, and the potential signaling pathways involved. A unilateral ureteral obstruction (UUO)‑induced renal fibrosis model was established using Sprague‑Dawley rats. Baicalin was administrated intraperitoneally every 2 days for 10 days. The degree of renal damage and fibrosis was investigated by histological assessment, and detection of fibronectin and collagen I mRNA expression levels. Epithelial‑mesenchymal transition (EMT) markers, transforming growth factor-β1 (TGF-β1) levels and downstream phosphorylation of mothers against decapentaplegic 2/3 (Smad2/3) were examined in vivo and in an NRK‑52E rat renal tubular cell line in vitro. Baicalin was demonstrated to markedly ameliorate renal fibrosis and suppress EMT, as evidenced by reduced interstitial collagen accumulation, decreased fibronectin and collagen I mRNA expression levels, upregulation of N‑ and E‑cadherin expression levels, and downregulation of α‑smooth muscle actin and vimentin expression. Furthermore, baicalin decreased TGF‑β1 expression levels in serum and kidney tissue following UUO, and suppressed Smad2/3 phosphorylation in rat kidney tissue. In vitro studies identified that baicalin may inhibit the phosphorylation of Smad2/3 under the same TGF‑β1 concentration. In conclusion, baicalin may protect against renal fibrosis, potentially via inhibition of TGF‑β1 production and its downstream signal transduction.
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Long
authors.initials: L
authors.lastname: Zheng
authors.affiliation: Shanghai Key Laboratory of Organ Transplantation, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Chao
authors.initials: C
authors.lastname: Zhang
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Long
authors.initials: L
authors.lastname: Li
authors.affiliation: Shanghai Key Laboratory of Organ Transplantation, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Chao
authors.initials: C
authors.lastname: Hu
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Mushuang
authors.initials: M
authors.lastname: Hu
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Niyazi
authors.initials: N
authors.lastname: Sidikejiang
authors.affiliation: Shanghai Key Laboratory of Organ Transplantation, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Xuanchuan
authors.initials: X
authors.lastname: Wang
authors.affiliation: Shanghai Key Laboratory of Organ Transplantation, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Miao
authors.initials: M
authors.lastname: Lin
authors.affiliation: Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032, P.R. China.
authors.forename: Ruiming
authors.initials: R
authors.lastname: Rong
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects; D005355:Fibrosis; D005419:Flavonoids / Q000494:pharmacology* / Q000627:therapeutic use*; D007150:Immunohistochemistry; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008954:Models, Biological; D010766:Phosphorylation / Q000187:drug effects; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects*; D051785:Smad Proteins / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis*; D014517:Ureteral Obstruction / Q000150:complications / Q000188:drug therapy / Q000473:pathology
chemical_list: D005419:Flavonoids; D051785:Smad Proteins; D053773:Transforming Growth Factor beta1; C038044:baicalin