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This is a mind map about medical discussion, including the main components of BSHXF are closely related to lipid metabolism\BSHXF treats POI by reducing menstrual lipid accumulation, etc.
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Medical discussion mind map
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
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- Reproductive development of animals
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- Outline
Summary of this article
POI is an important factor in infertility and seriously threatens women's quality of life. However, no specific drug has been proven to treat POI.
BSHXF is a clinical experience prescription with significant effect on the treatment of POI. However, the underlying reasons for BSHXF treatment of POI remain unclear.
In this article, our results show that BSHXF effectively reduces hormone secretion imbalance and follicle damage in the ovaries of POI rats. At the same time, in vivo and in vitro experimental data show that BSHXF treatment reduces ROS accumulation and excessive autophagy caused by lipid accumulation, thereby alleviating GC proliferation inhibition and apoptosis.
These findings suggest that BSHXF may be a superior drug candidate for the treatment of POI
The main components of BSHXF are closely related to lipid metabolism
BSHXT is composed of 11 traditional Chinese medicines with complex chemical composition. The top 23 compounds identified in this study have biological effects such as hypoglycemic, lipid-lowering, and antithrombotic effects. Among them, there are seven compounds with lipid-lowering effects. For example, paeoniflorin can not only reduce lipid accumulation and insulin resistance, but can also combine with liquiritigenin to reprogram lipid metabolism and improve neurological headaches. In addition, new mangiferin can also treat high-fat-induced non-alcoholic fatty liver disease.
Preliminary studies have found that BSHXF is the key metabolite of cholesterol lipids and triacylglycerols in treating ovarian hypofunction (DOR). (10.1016/j.heliyon.2023.e20104)
Our previous results of using proteomics to screen differential proteins also showed that the biological process of BSHXF improving POI regulation is concentrated in the lipid direction (TG homeostasis, negative regulation of TG metabolic processes, and negative regulation of lipase activity).
Therefore, BSHXF's treatment of POI may be related to its regulation of lipid metabolism.
BSHXF treats POI by alleviating lipid accumulation
Lipids and ovarian function
Lipids play an important role in maintaining ovarian function.
Fatty acids are energy providers in oocytes (Dunning et al, 2014)
Cholesterol is the precursor of steroid hormones synthesized in granulosa cells and theca cells.
However, excessive lipid accumulation can cause severe damage to ovarian function.
Excess adipose tissue accelerates the loss of ovarian follicles in rats by inhibiting SIRT1 signaling, leading to POF. (10.1016/j.arr.2022.101683)
During aging, the accumulation of free fatty acids (FFA) in the ovary is associated with oocyte mitochondrial dysfunction and cumulus-oocyte complex apoptosis, leading to decreased ovarian function. (10.3389/fcell.2022.806890)
BSHXF reduces lipid accumulation (results of this study)
In vivo study results show that BSHXF can significantly reduce lipid accumulation in the ovaries of POI rats, while reducing the expression of lipogenic proteins PPARγ and C/EBPα, and increasing the expression of lipolytic protein ATGL and lipid β-oxidation protein CPT1A.
In vitro studies have found that the free fatty acid PA can not only reduce E2 secretion in granulosa cells, but high concentrations of PA can also significantly promote the apoptosis of GCs. BSHXF can significantly improve these changes, and is consistent with the in vivo results. BSHXF reduces lipid production in GCs, promotes lipid degradation and oxidation, and alleviates lipid accumulation.
BSHXF reduces lipid accumulation-induced oxidative stress
Oxidative stress mediated by lipid accumulation is involved in the occurrence and development of various diseases (hepatitis, colon cancer, and arthritis); and studies have reported that excessive lipid accumulation can cause damage to ovarian function by inducing oxidative stress (10.1016 /j.redox.2022.102569).
This study found that BSHXF can significantly reduce lipid accumulation and ROS production in the ovaries of POI rats; at the same time, BSHXF can also significantly reverse the production of ROS in GCs induced by PA, and the therapeutic effect of BSHXF was reduced after adding ROS inducers. offset.
Therefore, BSHXF treatment of POI is related to its reduction of lipid production, promotion of lipid decomposition and oxidation, and thus reduction of ROS induced by lipid accumulation.
Outlook
Interestingly, studies have found that most women have increased cardiovascular risk factors (including weight gain, visceral obesity, and elevated blood lipids) after menopause, and it has been confirmed that premature menopause (primary ovarian insufficiency) The occurrence increases the patient's risk of developing atherosclerosis. In US guidelines, factors such as premature menopause are considered cardiovascular "risk-enhancing" factors, and statin therapy is recommended for women at borderline or intermediate risk (10.1093/eurheartj/ehad472).
Literature research found that rosuvastatin, resveratrol, curcumin and berberine, natural drugs with lipid-lowering biological activity that have entered clinical trials, all have a significant improvement effect on POI (10.1177/0960327119865588) .
Therefore, POI treatment drugs combined with lipid-lowering drugs may be a new strategy for the later treatment of POI. BSHXF takes into account both, and may be an advantageous drug candidate for late-stage POI treatment.
BSHXF treats POI by reducing excessive autophagy
Autophagy and ovarian function
In disease, autophagy has been described as a double-edged sword. On the one hand, autophagy contributes to cellular homeostasis by eliminating and recycling misfolded proteins or defective organelles (10.1016/j.cell.2007.12.018). On the other hand, excessive activation of autophagy is associated with cell proliferation and apoptosis resulting from excessive removal of organelles. (10.1016/j.freeradbiomed.2021.04.016)
Research shows that excessive autophagy induces the death of GCs (10.7150/ijbs.30369)
When humans are exposed to oxidized low-density lipoprotein, it will induce the accumulation of autophagosomes in GC, leading to cell death, and then leading to follicular atresia [10.1210/en.2006-0088].
In addition, ROS activates autophagy, reduces GCs cell proliferation and promotes GCs aging.
Drugs that reduce excessive autophagy improve POI
Human umbilical cord mesenchymal stem cells, melatonin, and hyperin can all improve POI by reducing autophagy. (10.1016/j.mito.2021.09.009, 10.1186/s13048-023-01278-z, 10.1016/j. biopha.2022.113743.)
The results of this study
BSHXF can reduce the accumulation of LC3 in POI rats and PA-induced GCs, promote the increase of P62, and alleviate excessive autophagy. However, after incubating BSHXF and autophagy inducers together, the anti-apoptotic effect of BHSXF on GCs and the E2 secretion function were reversed, while ROS inducers and autophagy inducers acted on GCs at the same time, and the anti-apoptotic effect of BSHXF on GCs And the E2 secretion function is completely canceled.
Study the points of conflict with others and analyze their causes
However, studies have reported that relieving the autophagy deficiency induced by cyclophosphamide is beneficial to the survival of GCs (10.1016/j.biopha.2022.113743).
Autophagy is dynamic and contributes differently to cell survival or death under different cellular conditions (10.1016/j.ceb.2009.11.015).
Studies have shown that insufficient autophagy can damage the differentiation of GCs and affect steroid secretion in antral follicles, thereby causing POI (10.1080/15548627.2022.2094671).
Therefore, the above situation may be due to the different ways we use to build the model, resulting in the different stages of GCs.
in conclusion
BSHXF can improve POI by alleviating excessive autophagy induced by lipid accumulation.
in conclusion
In conclusion, our research results show that BSHXF can improve POI by restoring ovarian hormone secretion and reducing follicular overactivation and atresia. Further studies have shown that BSHXF improves POI by reducing ROS and excessive autophagy induced by lipid accumulation (reducing lipid production, promoting lipid decomposition and oxidation). These results suggest that BSHXF may serve as a therapeutic agent for POI caused by metabolic disorders.
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