Dihydro-artemisinin inhibits angiotensin II-induced cardiac fibroblasts proliferation and induces apoptosis through phosphoinositide 3-kinase/akt pathway

IP: 8 46 247 10 On: Mon 07 Nov 2022 09:18:12 Cardiac fibroblasts (CFs) abnormal roliferation can triggr myocardial fibrosis, which is closely related to Copyright: American Scien ific Publishers a variety of cardiovascular diseases. This study investigated the effect of dihydroartemisinin (DHA) on CF Delivered by Ingenta growth through PI3K/AKT with angiotensin II (AngII). CCK-8 method and EdU were used detect cell prolifera-tion, and flow cytometry assessed apoptosis of CFs. The PI3K and AKT expressions were determined, whilst immunofluorescence staining and RT-qPCR measured a-smooth muscle actin (a-SMA) level. With rat CFs exhibiting typical fibroblast morphology and nuclei in spindle, oval or polygonal shape, these cells were posi-tive for the fibroblast marker vimentin. Treatment with AngII resulted in increased proliferation of CFs, but the proliferation declined in the presence of DHA (p < 0.05). Meanwhile, the AngII group had lower apoptosis of CFs than blank and DHA groups with highest apoptosis observed in the DHA group. a-SMA increased at the mRNA and protein levels after Ang II treatment and decreased after DHA treatment (p < 0.05). Importantly, the Ang II upregulated PI3K and AKT in CFs (p < 0.05) and the increase was abrogated by DHA adminis-tration with lowest levels (p < 0.05). Ang II activates PI3K/Akt in normal CFs, as administration of DHA can inhibit the effect of Ang II, thereby inhibiting proliferation of CFs induced by AngII and inducing apoptosis.

Automated summary

The study found that DHA can reduce the proliferation of CFs and induce apoptosis through inhibiting the PI3K/AKT pathway, thereby inhibiting myocardial fibrosis. This provides a new potential drug target and direction for the treatment of cardiovascular diseases.