[Effects of piperazine ferulate on TGF-beta1-induced renal interstitial fibroblast activation].
Guan-qiao You, Ping Fu, Xisheng Xie, Fei Liu, Jing Li
Abstract
Guan-qiao You, Ping Fu, Xisheng Xie, Fei Liu, Jing Li
Abstract
OBJECTIVE: To investigate the effects of piperazine ferulate (PF) on TGF-beta1-induced renal interstitial fibroblast activation, and to explore the mechanism of PF in the prevention of renal tubulointerstitial fibrosis. METHODS: In cultured normal rat renal kidney fibroblast (NRK-49F), the effect of PF on the TGF-beta1-induced cell vitality was observed by MTT. The protein expression levels of a-smooth muscle actin (alpha-SMA), connective tissue growth factor (CTGF) induced by TGF-beta1 were evaluated by immunocytochemistry. The levels of a-SMA, CTGF mRNA expression induced by TGF-beta1, were determined by quantitative real time fluroscent polymerase chain reaction. The levels of collagen type I (Col I) and fibronectin (FN) protein expression were examined by Enzyme Linked Immunosorbent Assay(ELISA). RESULTS: TGF-beta1 may markedly increase the cell vitality, alpha-SMA and CTGF expression, FN and Col I protein expression (P < 0.05). Compared with TGF-beta1-induced group, PF can partly decrease the cell vitality, level of alpha-SMA and CTGF expression and extracellular matrix(ECM) synthesis induced by TGF-beta1 (P < 0.05). CONCLUSION: PF may inhibit TGF-beta1-induced fibrosis in the renal fibroblast to a certain extent.
OpenAlex reports 2 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE: To investigate the effects of piperazine ferulate (PF) on TGF-beta1-induced renal interstitial fibroblast activation, and to explore the mechanism of PF in the prevention of renal tubulointerstitial fibrosis. METHODS: In cultured normal rat renal kidney fibroblast (NRK-49F), the effect of PF on the TGF-beta1-induced cell vitality was observed by MTT. The protein expression levels of a-smooth muscle actin (alpha-SMA), connective tissue growth factor (CTGF) induced by TGF-beta1 were evaluated by immunocytochemistry. The levels of a-SMA, CTGF mRNA expression induced by TGF-beta1, were determined by quantitative real time fluroscent polymerase chain reaction. The levels of collagen type I (Col I) and fibronectin (FN) protein expression were examined by Enzyme Linked Immunosorbent Assay(ELISA). RESULTS: TGF-beta1 may markedly increase the cell vitality, alpha-SMA and CTGF expression, FN and Col I protein expression (P < 0.05). Compared with TGF-beta1-induced group, PF can partly decrease the cell vitality, level of alpha-SMA and CTGF expression and extracellular matrix(ECM) synthesis induced by TGF-beta1 (P < 0.05). CONCLUSION: PF may inhibit TGF-beta1-induced fibrosis in the renal fibroblast to a certain extent.
Key concepts: CTGF, Fibronectin, Fibroblast, Extracellular matrix, Transforming growth factor, Chemistry, Fibrosis, Endocrinology