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Oxidized high-density lipoprotein enhances endocrine disorders and ovarian damage in rats.

ABSTRACT: Previous findings have highlighted the association between oxidized high-density lipoprotein (ox-HDL) and polycystic ovary syndrome (PCOS) development; however, the underlying mechanism remains unclear. Under such context, the present study aimed to investigate the mechanism underlying the involvement of ox-HDL in PCOS in relation to the p65/micro-RNA-34a (miR-34a)/FOS axis. PCOS rat models were established with the injection of dehydroepiandrosterone (6 mg/100 g body weight). Both PCOS-modelled rats and granulosa cells (GCs) were received treatment with ox-HDL in order to identify its role in PCOS. Next, apoptosis and viability of GCs were detected with the application of TdT-mediated dUTP Nick-End Labeling and flow cytometry and Cell counting kit-8, respectively. A series of assays were performed to determine the interaction among ox-HDL, p65, miR-34a, FOS and nuclear factor-κB (NF-κB). The results revealed high expression of ox-HDL in PCOS, and enhanced endocrine disorders and ovarian damage in rats. ox-HDL promoted apoptosis of GCs and decreased its viability. ox-HDL activated NF-κB pathway and induced p65 phosphorylation to promote miR-34a expression. miR-34a targeted and inhibited FOS expression. In conclusion, our findings suggested that ox-HDL promoted the activation of p65 and transcription of miR-34a, which stimulated apoptosis of GCs and inhibited expression of FOS, resulting in the overall acceleration of PCOS development.

SUBMITTER: Wang L

PROVIDER: S-EPMC8419193 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Apolipoproteins are associated with survival among patients on hemodialysis (HD), but these associations might be influenced by dysfunctional (oxidized) high-density lipoprotein (HDL). We assessed associations among apolipoproteins and oxidized HDL, mortality and cardiovascular disease (CVD) events in patients on HD. This prospective observational study examined 412 patients on prevalent HD. Blood samples were obtained before dialysis at baseline to measure lipids, apolipoproteins, oxidized LDL, oxidized HDL, high-sensitivity C-reactive protein (hs-CRP) and interleukin (IL)-6 at baseline, and HDL-C and hs-CRP were measured 12 months later. Patients were then prospectively followed-up (mean, 40 months) and all-cause mortality and composite CVD events were analyzed. Associations between variables at baseline and clinical outcome were assessed by Cox proportional hazards modeling (n = 412) and Cox hazards modeling with a time-varying covariate with HDL-C and hs-CRP (n = 369). Quartiles of apolipoproteins and oxidized HDL were not associated with all-cause mortality. However, Cox proportional hazards models with quartiles of each variable adjusted for confounders and hs-CRP or IL-6 identified apolipoprotein (apo)B-to-apoA-I ratio (apoB/apoA-I) and oxidized HDL, but not apoA-I or apoA-II, as independent risk factors for composite CVD events. These associations were confirmed by Cox proportional hazards modeling with time-varying covariates for hs-CRP. ApoB/apoA-I was independently associated with composite CVD events in 1-standard deviation (SD) increase-of-variables models adjusted for the confounders, oxidized HDL and hs-CRP. However, these associations disappeared from the model adjusted with IL-6 instead of hs-CRP, and oxidized HDL and IL-6 were independently associated with composite CVD events. Findings resembled those from Cox proportional hazards modeling using time-varying covariates with HDL-C adjusted with IL-6. In conclusion, both oxidized HDL and apoB/apoA-I might be associated with CVD events in patients on prevalent HD, while associations of apoB/apoA-I with CVD events differed between models of apoB/apoA-I quartiles and 1-SD increases, and were influenced by IL-6.

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Oxidized high-density lipoprotein enhances endocrine disorders and ovarian damage in rats.

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