New anti-cancer drugs are constantly being developed, especially targeted drugs. Although these drugs have achieved significant clinical efficacy, they do not play a significant role in ovarian cancer. Moreover, the research cycle and costs of such drugs are often huge. The repositioning of conventional drugs has gradually become a concern. Statins, as traditional lipid-lowering drugs, play a role mainly by inhibiting HMGCR. In recent years, epidemiological studies and in vitro experiments have confirmed its anti-cancer effect, especially the effect of anti-ovarian cancer. The mutation rate of TP53 in ovarian cancer is as high as 95%, while HMGCR is often highly expressed in TP53 mutant tumors. However, the effect of prospective clinical trials is not ideal. This result seems understandable considering that it seems unrealistic for a lipid-lowering drug to completely inhibit tumor growth. Therefore, statins play more synergistic roles in the treatment of ovarian cancer. Because ovarian cancer is a highly heterogeneous tumor, it may be a good choice to deeply understand the mechanism of statins in the treatment of ovarian cancer and achieve precise treatment by combining it with other drugs.
Chronic obstructive pulmonary disease (COPD) is a prevalent and long-term airway disease. It has been reported that fucoxanthin (FX) exhibits anti-inflammatory and antioxidant effects. However, the underlying mechanism of FX in COPD remains unknown. Therefore, to investigate the effect of FX on COPD, BEAS-2B cells were treated with cigarette smoke extract (CSE). The viability of BEAS-2B cells treated with increasing doses of FX was assessed by Cell Counting Kit-8. Lactate dehydrogenase (LDH) levels were measured using a corresponding kit. In addition, ELISA was carried out to detect the content of TNF-α, IL-1β and IL-6. Additionally, a TUNEL assay and western blot analysis were performed to assess the cell apoptosis rate. Furthermore, 2' ,7'-dichlorodihydrofluorescein diacetate was used to measure reactive oxygen species levels, while the contents of oxidative stress-associated indexes were determined using the corresponding kits. Bioinformatics analysis using the search tool for interactions of chemicals database predicted that peroxisome proliferator-activated receptor γ (PPARγ) may be a target of FX. The binding capacity of FTX with PPARγ was confirmed by molecular docking. The protein expression levels of the PPARγ/NF-κB signaling-associated factors were detected by western blot analysis. Finally, the regulatory mechanism of FX in COPD was revealed following cell treatment with the PPARγ inhibitor, T0070907. The results demonstrated that FX enhanced CSE-induced BEAS-2B cell viability and attenuated CSE-induced BEAS-2B cell inflammation and oxidative damage, possibly via triggering PPARγ/NF-κB signaling. Pre-treatment of BEAS-2B cells with the PPARγ inhibitor, T0070907, could reverse the protective effects of FX on CSE-induced BEAS-2B cells. Overall, the present study suggested that FX could ameliorate oxidative damage as well as inflammation in CSE-treated human bronchial epithelial in patients with COPD via modulating the PPARγ/NF-κB signaling pathway.
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