Objective. This investigation was conducted to analyze and evaluate the impact of Chinese herbal medicine on glucolipid metabolism in women with polycystic ovary syndrome (PCOS). Methods. We used manual and computer-aided search methods, and the search scopes included Chinese databases (China National Knowledge Infrastructure, Wanfang, the China Science and Technology Journal Database, and the Chinese Biomedical Literature Database) and English databases (PubMed, Embase, Web of Science, and the Cochrane Library). We searched these eight databases for randomized controlled trials investigating the effects of Chinese herbal medicine on glucolipid metabolism in women with PCOS, with the retrieval deadline being June 2021. Two reviewers screened, selected, and extracted data and verified the results independently. The NoteExpress software was used to manage and screen the literature, the risk of bias assessment tool was used to evaluate the methodological quality of the included studies, and the RevMan 5.4 software was used for meta-analysis. Results. A total of 13 trials were included, including 825 patients with PCOS. Because the drugs used in the control group were different, we divided the results into two parts, with four trials using placebo and nine trials using metformin as the control. The results of the meta-analysis showed that fasting insulin (MD=2.45, 95 CI=[4.74, 0.17], P=0.04), 2h fasting plasma glucose (MD=0.33, 95 CI=[0.64, 0.02], P=0.04), serum total cholesterol (MD=0.38, 95 CI=[0.58, 0.18], P=0.0002), triglycerides (MD=0.36, 95 CI=[0.58, 0.14], P=0.001), and low-density lipoprotein cholesterol (MD=0.58, 95 CI=[0.75, 0.41], P<0.00001) were significantly improved in the Chinese herbal medicine group compared with the placebo group. In addition, compared with metformin, body mass index (MD=1.04, 95 CI=[1.55, 0.53], P<0.0001), serum total cholesterol (MD=0.27, 95 CI=[0.46, 0.07] P=0.007), and low-density lipoprotein cholesterol were significantly reduced (MD=0.12, 95 CI=[0.22, 0.02], P=0.02) and high-density lipoprotein cholesterol (MD=0.09, 95 CI=[0.02, 0.17], P=0.01) was significantly improved after treatment with Chinese herbal medicine. Conclusion. Compared with the placebo group, Chinese herbal medicine had positive effects on glucolipid metabolism in women with PCOS. Chinese herbal medicine had a positive effect on lipid metabolism when the control group was metformin, but no effect on glucose metabolism. These findings need to be verified in high-quality, large-sample, randomized controlled trials in the future.

BACKGROUND: It has become evident that some women develop preeclampsia despite aspirin. This study aimed to examine how such aspirin nonresponsiveness develops in high-risk preeclampsia pregnancies by exploring the role of genetic polymorphisms and aspirin metabolism. METHODS: The study involved pregnant women who developed preeclampsia despite low-dose aspirin and those who did not. First, we conducted a pharmacogenomic association study exploring the association of potential genetic variants with aspirin nonresponsiveness. Next, we analyzed the rate of enzymatic aspirin hydrolysis in maternal plasma. The extent of placental exposure to acetylsalicylic acid and its bioactive metabolites, that is, salicylic acid and gentisic acid, was determined by liquid chromatography-mass spectrometry. The expressions of placental AMEs (aspirin metabolizing enzymes), that is, GLYAT (glycine-N-acyltransferase), UGT1A6 (UDP glucuronosyltransferase family 1 member A6), CYP2E1 (cytochrome P450 family 2 subfamily E member 1), and NAT2 (N-acetyltransferase 2) were analyzed by quantitative reverse transcription polymerase chain reaction, immunohistochemistry staining, and enzyme-linked immunosorbent assay. Finally, the effects of AMEs were further studied on HTR-8/SVneo (an immortalized human trophoblast cell line derived from first-trimester placenta) and hPCTB (human primary cytotrophoblast) cells. RESULTS: Our genetic study showed that single-nucleotide polymorphisms (SNPs) of genes involved in aspirin pharmacokinetics and pharmacodynamics were not associated with aspirin nonresponsiveness in preeclampsia. Rates of aspirin hydrolysis in maternal plasma and the concentrations of acetylsalicylic acid, salicylic acid, and gentisic acid in the placenta did not differ between aspirin-responsive and aspirin-nonresponsive women. Intriguingly, GLYAT was significantly upregulated in the aspirin-nonresponsive placenta and associated with aspirin nonresponsiveness. This overexpression of GLYAT was found to diminish the proangiogenic, anti-inflammatory, and antisenescence effects of salicylic acid in HTR-8/SVneo and hPCTB cells. CONCLUSIONS: Our study revealed that maternal genetic factors and plasma aspirin hydrolysis are not among the decisive factors in determining the effectiveness of low-dose aspirin in preventing preeclampsia among high-risk women. Instead, placental GLYAT appears to play a key role by limiting the effect of salicylic acid in the placenta.

The role of human leukocyte antigen F (HLA-F) at the maternal-fetal interface (MFI) during viral infection and its regulation by interferon signaling remains poorly understood. Here, we investigated HLA-F expression and regulation in first-trimester trophoblast cells following activation of the type I interferon pathway and viral infection. We demonstrate that HLA-F is significantly upregulated at both mRNA and protein levels in response to Poly(I:C) and IFN-β in a dose- and time-dependent manner, suggesting its regulation as an interferon-stimulated gene (ISG). Zika virus (ZIKV) infection similarly induced HLA-F upregulation over time. In contrast, HSV-2 infection downregulated HLA-F mRNA while maintaining steady protein levels, indicative of virus-specific regulatory mechanisms. Moreover, we identified a soluble HLA-F secreted following Poly(I:C) stimulation. These findings reveal that HLA-F is dynamically regulated in trophoblasts during viral challenge and type I IFN signaling activation, supporting its broader immunomodulatory role in antiviral defense and immune tolerance at the MFI.

The role of human leukocyte antigen F (HLA-F) at the maternal–fetal interface (MFI) during viral infection and its regulation by interferon signaling remains poorly understood. Here, we investigated HLA-F expression and regulation in first-trimester trophoblast cells following activation of the type I interferon pathway and viral infection. We demonstrate that HLA-F is significantly upregulated at both mRNA and protein levels in response to Poly(I:C) and IFN-β in a dose- and time-dependent manner, suggesting its regulation as an interferon-stimulated gene (ISG). Zika virus (ZIKV) infection similarly induced HLA-F upregulation over time. In contrast, HSV-2 infection downregulated HLA-F mRNA while maintaining steady protein levels, indicative of virus-specific regulatory mechanisms. Moreover, we identified a soluble form of HLA-F secreted following Poly(I:C) stimulation. These findings reveal that HLA-F is dynamically regulated in trophoblasts during viral challenge and type I IFN signaling activation, supporting its broader immunomodulatory role in antiviral defense and immune tolerance at the MFI.

Background/Objectives: Uterine dysfunction contributes to infertility in PCOS. Jiawei Qi Gong Wan (JQGW) is used to improve endometrial homeostasis, but its mechanism is unclear. This study investigated whether JQGW improves uterine function via gut microbiota and metabolites. Methods: Letrozole-induced PCOS mice received JQGW (low/high dose), metformin, or vehicle for 35 days. Endometrial morphology, receptivity genes, Akt2/NF-κB signaling, gut microbiota (16S rRNA), and serum metabolites (LC-MS) were assessed. Results: PCOS mice showed reduced endometrial thickness (126.4 ± 10.8 μm vs. 215.6 ± 12.3 μm in controls, p < 0.001) and fewer glands (12.6 ± 1.8 vs. 28.4 ± 2.1, p < 0.001). JQGW-H increased endometrial thickness (189.3 ± 11.2 μm, p < 0.01 vs. PCOS) and gland number (23.1 ± 1.9, p < 0.01 vs. PCOS), restored the receptivity markers (Nr2f2, Pc6, Ptch, and Hbegf) toward normal levels, suppressed Akt2/NF-κB activation, and reduced inflammatory cytokines. JQGW shifted the β-diversity structure of the gut microbiota toward the control pattern, with Oscillospira enrichment (LDA > 4). Four metabolites (PA(20:0/16:1(9Z)), 7-methylguanosine, methoxyacetic acid, 8.11-eicosadiynoic acid) showed nominal elevation in PCOS and negative correlations with endometrial thickness (r = −0.73 to −0.89, unadjusted p < 0.01), although none survived FDR correction. Conclusions: JQGW ameliorates PCOS-associated uterine dysfunction, potentially via gut microbiota and metabolite modulation. Future studies should validate causality using fertility-based outcomes and microbiota transplantation.