Corilagin Alleviates Ang II-Induced Cardiac Fibrosis by Regulating the PTEN/AKT/mTOR Pathway

Area of Science:

• Cardiovascular Research
• Pharmacology
• Cell Biology

Background:

• Cardiac fibrosis is a significant contributor to heart failure.
• Angiotensin II (Ang II) is a key mediator in the development of cardiac fibrosis.
• Identifying effective therapeutic agents against Ang II-induced cardiac fibrosis is crucial.

Purpose of the Study:

• To investigate the therapeutic potential of corilagin (Cor) in mitigating Ang II-induced cardiac fibrosis.
• To elucidate the underlying molecular mechanisms of Cor's protective effects.

Main Methods:

• C57BL/6 mice were treated with Ang II to induce cardiac fibrosis.
• Corilagin (Cor) was administered intraperitoneally to assess its therapeutic effects.
• Key fibrotic markers, oxidative stress indicators, and signaling pathway proteins (PTEN/AKT/mTOR) were analyzed.

Main Results:

• Cor treatment significantly reduced cardiac fibrotic area and fibroblast proliferation induced by Ang II.
• Cor inhibited the expression of fibrotic markers (α-SMA, collagen I, III, TGF-β1, CTGF, fibronectin).
• Cor suppressed reactive oxygen species (ROS) and malondialdehyde (MDA), while increasing superoxide dismutase (SOD) and catalase (CAT) activity.
• Cor reduced the phosphorylation of PTEN, AKT, and mTOR, and inhibited cardiac fibroblast migration.

Conclusions:

• Corilagin demonstrates significant protective effects against Ang II-induced cardiac fibrosis.
• Corilagin's mechanism involves the inhibition of the PTEN/AKT/mTOR signaling pathway.
• Corilagin represents a promising therapeutic candidate for managing cardiac fibrosis.