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Objective: Follicle-stimulating hormone (FSH) level changes may be another reason for increasing the risk of cardiovascular disease. In this study, we aimed to investigate the role of FSH in atherosclerosis and its underlying mechanism. Methods: ApoE−/− mice were divided into 4 groups, namely, the sham group, bilaterally orchidectomized group, FSH group, and testosterone-only group. Blood lipid and hormone levels were tested, aorta Oil Red O staining; the levels of NF-κB, Akt, eNOS, and FSH receptors in the aorta were measured by Western blotting. Expression of VCAM-1 was detected via Western blotting and immunohistochemical staining. Human umbilical vein endothelial cells (HUVECs) were used to induce endothelial injury model by adding FSH, and the levels of NF-κB, Akt, eNOS, and FSHR were tested in HUVECs. Results: FSH treatment exacerbated atherosclerotic lesions in ApoE−/− mice. Moreover, FSH could promote the expression of VCAM-1 protein in HUVECs, and this effect was possibly mediated by the activation of NF-κB, while NF-κB activation was further enhanced by the activation of the PI3K/Akt/eNOS pathway. FSH failed to activate Akt and NF-κB in the presence of the PI3K inhibitor LY294002 in HUVECs. Conclusion: FSH promoted the development of atherosclerosis by increasing VCAM-1 protein expression via activating PI3K/Akt/NF-κB pathway. [ABSTRACT FROM AUTHOR]

The objective of this work was to study the lipid profile (LDL, TC, TG, and HDL) over 2 years in patients with hyperlipidemia in a real-world clinical setting and to describe the dynamical trajectory of lipid profile change in response to lipid-lowering treatment (Zhenzhu Tiaozhi capsule (FTZ) vs. general lipid-lowering treatment, i.e., statins, fibrates, and Xuezhikang). We conducted a retrospective study that included people aged ≥18 years with hyperlipidemia that initiated lipid-lowering treatment between January 2010 and December 2020. Demographic, diagnosis, and laboratory data were retrieved from hospital's electronic medical records, including hospital information system (HIS) and the laboratory information system (LIS). Follow-up trajectories of lipid profile were plotted in a generalized additive mixed model (GAMM) with smooth splines. A total of 839 patients with hyperlipidemia were included. Within 2 years, LDL, TC, and TG descended steadily and gently in the FTZ group (N = 99), while the general lipid-lowering treatment (N = 740) shortly improved LDL, TC, and TG before 11 weeks and was no longer present around 30 weeks. After 30 weeks, the trajectory of LDL, TC, and TG fluctuated up and down. Also, for HDL, a similar trajectory was observed before 40 weeks between 2 groups, but the FTZ group showed an increasing trend after 40 weeks, while a similar trend was not seen in the general lipid-lowering group. In this study, FTZ was shown to have similar long-term effectiveness as an alternative lipid-lowering treatment to the general lipid-lowering treatment. The findings of this study provide observational evidence for further studies of FTZ, but more prospective studies are needed to determine the impacts of FTZ on lipid profile. [ABSTRACT FROM AUTHOR]