Thus, CXCL4/CXCR3-B may be involved in the mechanism of apoptosis induced by paeonol in breast cancer cells by regulating the expression of BACH1 and Nrf2 to downregulating HO-1 and promote apoptosis. Therefore, the authors suggest paeonol has a significant growth inhibitory effect on breast cancer cells, which may be related to the induction of apoptosis.
Background/aim: Hexarelin is a synthetic growth hormone-releasing peptide that exerts cardioprotective effects. However, its cardioprotective effect against heart failure (HF) is yet to be explained. This study investigated the therapeutic role of hexarelin and the mechanisms underlying its cardioprotective effects against coronary artery ligation (CAL)-induced HF in rats.Materials and methods: Rats with four weeks of permanent CAL, induced myocardial infarction, and HF were randomly separated into four groups: the control group (Ctrl), sham group (Sham), hexarelin treatment group (HF + Hx), and heart failure group (HF). The rats were treated with subcutaneous injection of hexarelin (100 µg/kg) in the treatment group or saline in the other groups twice a day for 30 days. Left ventricular (LV) function, oxidative stress, apoptosis, molecular analyses, and cardiac structural and pathological changes in rats were assessed.
Results:The treatment of HF rats with hexarelin significantly induced the upregulation of phosphatase and tensin homologue (PTEN) expression and inhibited the phosphorylation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR) to significantly improve LV function, ameliorate myocardial remodeling, and reduce oxidative stress.
Conclusion:These findings indicate that hexarelin attenuates CAL-induced HF in rats by ameliorating myocardial remodeling, LV dysfunction, and oxidative stress via the upmodulation of PTEN signaling and downregulation of the Akt/mTOR signaling pathway.
Phyllanthus urinaria has been characterized for its several biological and medicinal effects such as antiviral, antibacterial, anti-inflammatory, anticancer, and immunoregulation. In recent years, Phyllanthus urinaria has demonstrated potential to modulate the activation of critical pathways such as NF-κB, P13K/AKT, and ERK/JNK/P38/MAPKs associated with cell growth, proliferation, metastasis, and apoptotic cell death. To date, there is much evidence indicating that modulation of cellular signaling pathways is a promising approach to consider in drug development and discovery. Thus, therapies that can regulate cancer-related pathways are longed-for in anticancer drug discovery. This review’s focus is to provide comprehensive knowledge on the anticancer mechanisms of Phyllanthus urinaria through the regulation of NF-κB, P13K/AKT, and ERK/JNK/P38/MAPKs signaling pathways. Thus, the review summarizes both in vitro and in vivo effects of Phyllanthus urinaria extracts or bioactive constituents with emphasis on tumor cell apoptosis. The literature information was obtained from publications on Google Scholar, PubMed, Web of Science, and EBSCOhost. The key words used in the search were “Phyllanthus” or “Phyllanthus urinaria” and cancer. P. urinaria inhibits cancer cell proliferation via inhibition of NF-κB, P13K/AKT, and MAPKs (ERK, JNK, P38) pathways to induce apoptosis and prevents angiogenesis. It is expected that understanding these fundamental mechanisms may help stimulate additional research to exploit Phyllanthus urinaria and other natural products for the development of novel anticancer therapies in the future.
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