Importance: The incidence of dyslipidemia increases after menopause. Menopause hormone therapy (MHT) is recommended for menopause related disease. However, it is benefit for lipid profiles is inconclusive.Objective: To conduct a systematic review and meta-analysis of randomized controlled trials to evaluate the effects of MHT on lipid profile in postmenopausal women.Evidence Review: Related articles were searched on PubMed/Medline, EMBASE, Web of Science, and Cochrane Library databases from inception to December 2020. Data extraction and quality evaluation were performed independently by two reviewers. The methodological quality was assessed using the “Cochrane Risk of Bias checklist”.Results: Seventy-three eligible studies were selected. The results showed that MHT significantly decreased the levels of TC (WMD: −0.43, 95% CI: −0.53 to −0.33), LDL-C (WMD: −0.47, 95% CI: −0.55 to −0.40) and LP (a) (WMD: −49.46, 95% CI: −64.27 to −34.64) compared with placebo or no treatment. Oral MHT led to a significantly higher TG compared with transdermal MHT (WMD: 0.12, 95% CI: 0.04–0.21). The benefits of low dose MHT on TG was also concluded when comparing with conventional-dose estrogen (WMD: −0.18, 95% CI: −0.32 to −0.03). The results also showed that conventional MHT significantly decreased LDL-C (WMD: −0.35, 95% CI: −0.50 to −0.19), but increase TG (WMD: 0.42, 95%CI: 0.18–0.65) compared with tibolone. When comparing with the different MHT regimens, estrogen (E) + progesterone (P) regimen significantly increased TC (WMD: 0.15, 95% CI: 0.09 to 0.20), LDL-C (WMD: 0.12, 95% CI: 0.07–0.17) and Lp(a) (WMD: 44.58, 95% CI:28.09–61.06) compared with estrogen alone.Conclusion and Relevance: MHT plays a positive role in lipid profile in postmenopausal women, meanwhile for women with hypertriglyceridemia, low doses or transdermal MHT or tibolone would be a safer choice. Moreover, E + P regimen might blunt the benefit of estrogen on the lipid profile.Clinical Trial Registration: [https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42018092924], identifier [No. CRD42018092924].

Huyang Yangkun Formula(HYF) is a traditional Chinese medicine formula based on the traditional theory of Yin and Yang. It could consolidate the Qi of Yin and Yang, adjust the balance of Qi and blood. It has shown clinical efficacy for patients with Premature Ovarian Insufficiency(POI). Aim to access the effect of Huyang Yangkun formula (HYF) on premature ovarian insufficiency rat model and explores the mechanism related to aquaporins(AQPs) and apoptosis. Female SD rats were injected with 4-vinylcyclonhexenediepoxide(VCD, 160 mg/kg/day) for 15 days. Then, HYF (0.297 g/kg)/estradiol valerate (0.1 mg/kg) was administered for 105 days in the HYF/estradiol valerate treatment(EVT) group. Serum AMH, FSH and E₂ were detected by ELISA, and the developing follicles were counted in each group.The TUNEL assay was used to detect positive apoptotic signals. IHC and western blots were used to verify differentially expressed AQPs and apoptosis-related regulators potentially associated with HYF. Total follicles were increased significantly in the HYF group. Serum AMH was increased in the HYF group compared with MOD group. Serum FSH and E₂ showed no obvious difference between HYF group and MOD group. Apoptosis occurred in POI model was proved by TUNEL and Caspase3/9 and HYF could rescue this apoptosis, besides the anti-apoptotic effect may be better than EVT. Distribution of AQPs in rat ovaries based on developmental stages of follicle was observed, and AQP8 was obviously expressed in the developing follicles and corpus luteum, particularly in granulosa cells. Upregulation of AQP8 in the MOD group and downregulation by HYF were observed. BCL-XL was significantly upregulated in the HYF group and EVT group; BCL-2 was upregulated in the HYF group with no statistical difference; MCL-1 was downregulated in the HYF group. BAX and BIM were significantly upregulated in the MOD group. The ratio of BCL-2/BAX and BCL-XL/BAX were decreased in the MOD group, and BCL-XL/BAX was increased in the HYF group and EVT group. This study evaluated the treatment effect of HYF on POI in rats. It showed that HYF could promote the follicles development by regulating AQP8/Bcl-2 family-related mitochondrial apoptosis, which provides basic evidence for TCM as an alternative therapy for POI.

This study aimed to analyze the effectiveness of acupuncture combined with Chinese herbal medicine (CHM) on mood disorder symptoms for menopausal women.A total of 95 qualified Chinese participants ...

Background: Management of menopausal dyslipidemia is the main measure to reduce the incidence of cardiovascular disease in postmenopausal women. Tonifying Kidney and Removing Dampness Formula (TKRDF) is a traditional Chinese medicine (TCM) formula that ameliorates dyslipidemia in postmenopausal women. This study applied network pharmacology, molecular docking, and in vitro and in vitro experiments to investigate the underlying mechanism of TKRDF against postmenopausal dyslipidemia.Methods: Network pharmacology research was first conducted, and the active compounds and targets of TKRDF, as well as the targets of postmenopausal dyslipidemia, were extracted from public databases. Protein–protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used to identify the potential targets and signaling pathways of TKRDF in postmenopausal dyslipidemia. Molecular docking was then performed to evaluate the combination of active compounds with principal targets. Finally, an ovariectomized rat model was used for the in vivo experiment and alpha mouse liver 12 (AML12) cells treated with palmitic acid were used for the in vitro experiments to provide further evidence for the research.Results: Based on network pharmacology analysis, we obtained 78 active compounds from TKRDF that acted on 222 targets of postmenopausal dyslipidemia. The analysis results indicated that IL6, TNF, VEGFA, AKT1, MAPK3, MAPK1, PPARG and PIK3CA, etc., were the potentially key targets, and the PI3K/AKT signaling pathway was the possibly crucial pathway for TKRDF to treat postmenopausal dyslipidemia. Molecular docking suggested that the active compounds have good binding activity with the core targets. The in vivo and in vitro experiments demonstrated that TKRDF ameliorates postmenopausal dyslipidemia by regulating hormone levels, inhibiting inflammation, promoting angiogenesis and inhibiting lipid synthesis, which appear to be related to TKRDF’s regulation of the ERK1/2 and PI3K/AKT signaling pathways.Conclusion: This study clarified the active ingredients, potential targets, and molecular mechanisms of TKRDF for treating postmenopausal dyslipidemia. It also provided a feasible method to uncover the scientific basis and therapeutic mechanism for prescribing TCM in the treatment of diseases.

Non-alcoholic fatty liver disease (NAFLD) has becomeserious liverdisease all over the world. At present, NAFLD caused by high calorieand fat diet is increasing. Calsyntenin-3 (Clstn3) is a transmembraneprotein that has recently been found to participate in lipid energymetabolism. But whether Clstn3 affects NAFLD lipid metabolism hasnot been analyzed. We stimulate the mice primary hepatocytes (MPHs)with oleic acid and palmitic acid (OA & PA) to establish a cellmodel. Then, potential targets, including Clstn3 gene, were validatedfor improving lipid metabolism disorder in NAFLD model mice (HFD anddb/db) by silencing and overexpressing hepatic Clstn3. Moreover, theeffects of Clstn3 on lipid homeostasis were determined by functionaldetermination, triglyceride (TG) levels, total cholesterol (TC) levels,ELISA, and qRT-PCR detection. Our results displayed that Clstn3 wasdecreased in the NAFLD mice model. Also, overexpression of Clstn3improved lipid metabolism disorders, gluconeogenesis, and energy homeostasisand reduced liver injury, inflammation, and oxidative stress injury.However, opposite results were obtained in Clstn3-silencing mice,suggesting that the Clstn3 gene is closely related to lipid metabolismdisorder in NAFLD. RNAseq expression demonstrated that Farnesoid XReceptor (FXR) expression was increased after overexpression of Clstn3.Clstn3 supplementation in FXRKO mice can improve the dysfunction causedby insufficient FXR, suggesting that Clstn3 can improve the NAFLDlipid metabolism disorder to some extent through FXR, which may providea new method for the treatment of NAFLD.