Abstract Title:

Asiatic acid inhibits cardiac fibrosis throughNrf2/HO-1 and TGF-β1/Smads signaling pathways in spontaneous hypertension rats.

Abstract Source:

Int Immunopharmacol. 2019 Jun 26 ;74:105712. Epub 2019 Jun 26. PMID: 31254954

Abstract Author(s):

Zhe Meng, Hai-Yu Li, Chun-Ying Si, Yu-Zhou Liu, Shuai Teng

Article Affiliation:

Zhe Meng


OBJECTIVE: Asiatic acid (AA) has been suggested to inhibit pulmonary and hepatic fibrosis, while its influence on cardiac fibrosis remains unclear. We aimed to investigate whether AA could inhibit overpressure-induced cardiac fibrosis in spontaneous hypertension rats (SHRs).

METHOD: SHRs were treated with AA (20 mg kg day) for 12 weeks and cultured cardiac fibroblasts (CFs) were treated with Ang II (10 mol/L) in vitro. Markers of oxidative stress were measured and extent of cardiac fibrosis was evaluated with Sirius Red staining. Levels of Superoxide Dismutase (SOD), Malondialdehyde (MDA), reactive oxygen spices (ROS) and Glutathione (GSH) were measured by using commercial assay kits. Collagendeposition was detected. The expression of relative protein and mRNA was measured by Western blot and real-time PCR, respectively.

RESULTS: AA reduced systolic blood pressure, attenuated myocardial hypertrophy, reduced college deposition and the expression of collagen I and III, connective tissue growth factor, and plasminogen activator inhibitor-1, in mRNA and protein levels, with inhibition of TGF-β1 expression, phosphorylation of Smad2/3, and increase of Smad7 expression. AA reduced malondialdehyde and reactive oxygen spices, while increased the activities of superoxide dismutase and glutathione, accompanied with elevation of nuclear translocation of nuclear-factor erythroid 2-related factor 2 (Nrf2) and expression of heme oxygenase (HO-1) and NAD(P)H dehydrogenase [quinone] 1 (NQO-1) in vivo and in vitro. Moreover, pretreating CFs with siRNA for Smad7 or Nrf2 both partially reversed the inhibition of AA on Ang II-induced cardiac fibrosis.

CONCLUSION: AA attenuates pressure overload-induced cardiac fibrosis via enhancing of Nrf2/HO-1 and suppressing TGF-β1/Smads phosphorylation.

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