[Alisol B inhibited complement 3a-induced human renal tubular epithelial to mesenchymal transition]

Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Oct;32(10):1407-12.
[Article in Chinese]

Abstract

Objective: To study whether alisol B could inhibit complement 3a (C3a) induced renal tubular epithelial-mesenchymal transition (EMT).

Methods: The in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-beta (TGF-beta), 0.1 micromol C3a, and 0.1 micromol C3a + 10 micromol alisol B, respectively. The mRNA and protein expressions of alpha-SMA, E-cadherin, and C3 were detected using RT-PCR, Western blot, and immunofluorescence, respectively.

Results: The mRNA and protein expressions of C3 in HK-2 cells were up-regulated after intervention of C3a (P < 0.01), the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously enhanced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously decreased (P < 0.01). When compared with the group intervened by exogenous C3a, after intervention of alisol B, the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously reduced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously increased (P < 0.05).

Conclusions: Exogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Antigens, CD
  • Cadherins / metabolism
  • Cell Differentiation / drug effects
  • Cell Line
  • Cholestenones / pharmacology*
  • Complement C3a / metabolism
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Epithelial-Mesenchymal Transition / drug effects*
  • Humans
  • Kidney Tubules / cytology*
  • Kidney Tubules / metabolism

Substances

  • Actins
  • Antigens, CD
  • CDH1 protein, human
  • Cadherins
  • Cholestenones
  • alisol B
  • Complement C3a