Long noncoding RNA protein-disulfide isomerase-associated 3 regulated high glucose-induced podocyte apoptosis in diabetic nephropathy through targeting miR-139-3p.

BACKGROUND: Podocyte apoptosis plays a vital role in proteinuria pathogenesis in diabetic nephropathy (DN). The regulatory relationship between long noncoding RNAs (lncRNAs) and podocyte apoptosis has recently become another research hot spot in the DN field. AIM: To investigate whether lncRNA protein-disulfide isomerase-associated 3 (Pdia3) could regulate podocyte apoptosis through miR-139-3p and revealed the underlying mechanism. METHODS: Using normal glucose or high glucose (HG)-cultured podocytes, the cellular functions and exact mechanisms underlying the regulatory effects of lncRNA Pdia3 on podocyte apoptosis and endoplasmic reticulum stress (ERS) were explored. LncRNA Pdia3 and miR-139-3p expression were measured through quantitative real-time polymerase chain reaction. Relative cell viability was detected through the cell counting kit-8 colorimetric assay. The podocyte apoptosis rate in each group was measured through flow cytometry. The interaction between lncRNA Pdia3 and miR-139-3p was examined through the dual luciferase reporter assay. Finally, western blotting was performed to detect the effect of lncRNA Pdia3 on podocyte apoptosis and ERS via miR-139-3p. RESULTS: The expression of lncRNA Pdia3 was significantly downregulated in HG-cultured podocytes. Next, lncRNA Pdia3 was involved in HG-induced podocyte apoptosis. Furthermore, the dual luciferase reporter assay confirmed the direct interaction between lncRNA Pdia3 and miR-139-3p. LncRNA Pdia3 overexpression attenuated podocyte apoptosis and ERS through miR-139-3p in HG-cultured podocytes. CONCLUSION: Taken together, this study demonstrated that lncRNA Pdia3 overexpression could attenuate HG-induced podocyte apoptosis and ERS by acting as a competing endogenous RNA of miR-139-3p, which might provide a potential therapeutic target for DN.

The pH-Induced Increase of the Rate Constant for HER at Au(111) in Acid Revealed by Combining Experiments and Kinetic Simulation.

Origins of pH effects on the kinetics of electrocatalytic reactions involving the transfer of both protons and electrons, including the hydrogen evolution reaction (HER) considered in this study, are heatedly debated. By taking the HER at Au(111) in acid solutions of different pHs and ionic concentrations as the model systems, herein, we report how to derive the intrinsic kinetic parameters of such reactions and their pH dependence through the measurement of j-E curves and the corresponding kinetic simulation based on the Frumkin-Butler-Volmer theory and the modified Poisson-Nernst-Planck equation. Our study reveals the following: (i) the same set of kinetic parameters, such as the standard activation Gibbs free energy, charge transfer coefficient, and Gibbs adsorption energy for Had at Au(111), can simulate well all the j-E curves measured in solutions with different pH and temperatures; (ii) on the reversible hydrogen electrode scale, the intrinsic rate constant increases with the increase of pH, which is in contrast with the decrease of the HER current with the increase of pH; and (iii) the ratio of the rate constants for HER at Au(111) in x M HClO4 + (0.1 - x) M NaClO4 (pH ≤ 3) deduced before properly correcting the electric double layer (EDL) effects to the ones estimated with EDL correction is in the range of ca. 10 to 40, and even in a solution of x M HClO4 + (1 - x) M NaClO4 (pH ≤ 2) there is a difference of ca. 5× in the rate constants without and with EDL correction. The importance of proper correction of the EDL effects as well as several other important factors on unveiling the intrinsic pH-dependent reaction kinetics are discussed to help converge our analysis of pH effects in electrocatalysis.

Divergent trajectory of replication and intrinsic pathogenicity of SARS-CoV-2 Omicron post-BA.2/5 subvariants in the upper and lower respiratory tract.

BACKGROUND: Earlier Omicron subvariants including BA.1, BA.2, and BA.5 emerged in waves, with a subvariant replacing the previous one every few months. More recently, the post-BA.2/5 subvariants have acquired convergent substitutions in spike that facilitated their escape from humoral immunity and gained ACE2 binding capacity. However, the intrinsic pathogenicity and replication fitness of the evaluated post-BA.2/5 subvariants are not fully understood. METHODS: We systemically investigated the replication fitness and intrinsic pathogenicity of representative post-BA.2/5 subvariants (BL.1, BQ.1, BQ.1.1, XBB.1, CH.1.1, and XBB.1.5) in weanling (3-4 weeks), adult (8-10 weeks), and aged (10-12 months) mice. In addition, to better model Omicron replication in the human nasal epithelium, we further investigated the replication capacity of the post-BA.2/5 subvariants in human primary nasal epithelial cells. FINDINGS: We found that the evaluated post-BA.2/5 subvariants are consistently attenuated in mouse lungs but not in nasal turbinates when compared with their ancestral subvariants BA.2/5. Further investigations in primary human nasal epithelial cells revealed a gained replication fitness of XBB.1 and XBB.1.5 when compared to BA.2 and BA.5.2. INTERPRETATION: Our study revealed that the post-BA.2/5 subvariants are attenuated in lungs while increased in replication fitness in the nasal epithelium, indicating rapid adaptation of the circulating Omicron subvariants in the human populations. FUNDING: The full list of funding can be found at the Acknowledgements section.

IrO2 as a promising support to boost oxygen reduction reaction on Pt in acid under high temperature conditions.

Metal oxide nanoparticle (NP) supports of both good conductivity and stability have the potential to enhance both the reaction activity and stability of the loaded electrocatalysts. In this paper, a facile two-step approach to disperse Pt nanoparticles on the surface of an IrO2 NP support (Pt/IrO2) was developed. Physical characterization by x-ray diffraction spectroscopy and transmission/scanning electron microscopy suggests a good dispersion of the Pt NPs. The temperature effect (from 293 to 353 K) of oxygen reduction reaction on Pt/IrO2 was studied by using a rotating ring disk electrode The results show that although the kinetic current density on Pt/IrO2 is close to that on commercial Pt/C at room temperature, the apparent activation energy (Ea,app) in the former case is much lower, suggesting a much higher activity at elevated temperatures. The superiority in Ea,app is attributed to the electron interaction between Pt and the IrO2 support, as supported by the change of surface chemical state given by x-ray photo-electron spectroscopy.

Analysis of the impact of peritoneal dialysis catheter tail-end design on catheter-related complications.

OBJECTIVE: Evaluate the impact of peritoneal dialysis catheter (PDC) tail-end design variations on PDC-related complications. METHOD: Effective data were extracted from databases. The literature was evaluated according to the Cochrane Handbook for Systematic Reviews of Interventions, and a meta-analysis was conducted. RESULTS: Analysis revealed that the straight-tailed catheter was superior to the curled-tailed catheter in minimizing catheter displacement and complication-induced catheter removal (RR = 1.73, 95%CI:1.18-2.53, p = 0.005). In terms of complication-induced PDC removal, the straight-tailed catheter was superior to the curled-tailed catheter (RR = 1.55, 95%CI: 1.15-2.08, p = 0.004). CONCLUSION: Curled-tail design of the catheter increased the risk of catheter displacement and complication-induced catheter removal, whereas the straight-tailed catheter was superior to the curled-tailed catheter in terms of reducing catheter displacement and complication-induced catheter removal. However, the analysis and comparison of factors such as leakage, peritonitis, exit-site infection, and tunnel infection did not reveal a statistically significant difference between the two designs.

The electrostatic effect and its role in promoting electrocatalytic reactions by specifically adsorbed anions.

The adsorption of anions and its impact on electrocatalytic reactions are fundamental topics in electrocatalysis. Previous studies revealed that adsorbed anions display an overall poisoning effect in most cases. However, for a few reactions such as the hydrogen evolution reaction (HER), oxidation of small organic molecules (SOMs), and reduction of CO2 and O2, some specifically adsorbed anions can promote their reaction kinetics under certain conditions. The promotion effect is frequently attributed to the adsorbate induced modification of the nature of the active sites, the change of the adsorption configuration and free energy of the key reactive intermediate which consequently change the activation energy, the pre-exponential factor of the rate determining step etc. In this paper, we will give a mini review of the indispensable role of the classical double layer effect in enhancing the kinetics of electrocatalytic reactions by anion adsorption. The ubiquitous electrostatic interactions change both the potential distribution and the concentration distribution of ionic species across the electric double layer (EDL), which alters the electrochemical driving force and effective concentration of the reactants. The contribution to the overall kinetics is highlighted by taking HER, oxidation of SOMs, reduction of CO2 and O2, as examples.

MiR-449a downregulation alleviates the progression of renal interstitial fibrosis by mediating the KLF4/MFN2 axis.

BACKGROUND: Renal interstitial fibrosis (RIF) seriously threatens the health of individuals. MiRNAs regulate the progression of fibrosis. Nevertheless, the detailed function of miR-449a in RIF is largely unknown. METHODS: In vitro and in vivo models of RIF were developed to evaluate the function of miR-449a. The relationship among miR-449a, KLF4, and MFN2 was explored using a dual-luciferase reporter assay and chromatin immunoprecipitation. Additionally, the pathological changes in the mice were detected using Masson staining. The mRNA and protein expressions were assessed using quantitative reverse transcription polymerase chain reaction and western blot, respectively. RESULTS: TGF-ß1 downregulated the expressions of KLF4 and MFN2 in TCMK-1 cells, but upregulated the level of miR-449a. The downregulation of miR-449a significantly inhibited TGF-ß1-induced upregulation of fibrotic proteins in TCMK-1 cells. Meanwhile, miR-449a directly targeted KLF4. Moreover, KLF4 overexpression activated MFN2 transcription and reversed TGF-ß1-induced fibrosis by positively regulating MFN2. Furthermore, the downregulation of miR-449a could obviously alleviate the symptoms of RIF in mice with unilateral ureteral obstruction. CONCLUSION: MiR-449a downregulation attenuated the development of RIF by mediating the KLF4/MFN2 axis. Therefore, miR-449a might act as a target in treating RIF.

LncRNA NEAT1 accelerates renal fibrosis progression via targeting miR-31 and modulating RhoA/ROCK signal pathway.

Renal fibrosis is the final pathway for chronic kidney disease to end-stage renal failure. Noncoding RNAs have been reported to play a crucial role in renal fibrosis. Here, the effects of long noncoding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) and miR-31 on renal fibrosis and their regulatory mechanism were evaluated. RT-qPCR was used to assess NEAT1, miR-31, and RhoA levels. Western blot was performed to analyze the expression of fibrosis markers, RhoA, rho-related kinase (ROCK1), and connective tissue growth factor (CTGF). RNA immunoprecipitation (RIP), fluorescence in situ hybridization (FISH), and luciferase reporter assays verified the interaction between miR-31 and NEAT1 or RhoA. Renal fibrosis and injury were observed by Masson and hematoxylin and eosin (H&E) staining. The expression level of inflammatory cytokines was detected by ELISA. Immunohistochemistry (IHC) was performed to examine the expression levels of α-smooth muscle actin (α-SMA) and RhoA in renal tissues. We showed that NEAT1 was highly expressed, whereas miR-31 was decreased in renal fibrosis. NEAT1 was found to directly bind miR-31 to positively regulate RhoA expression. Furthermore, NEAT1 silencing inhibited renal fibrosis and inflammation and suppressed the RhoA/ROCK1 signaling pathway. However, knockdown of miR-31 could reverse these effects. NEAT1 silencing or overexpression of miR-31 alleviated renal fibrosis in vivo. In conclusion, NEAT1 accelerates renal fibrosis progression via negative regulation of miR-31 and the activation of RhoA/ROCK1 pathway, thereby upregulating the expression level of CTGF, providing a theoretical basis for treatment and prognostic evaluation of renal fibrosis.

Clinical study on the use of advanced magnetic resonance imaging in lupus nephritis.

OBJECTIVES: To investigate the correlation between the histopathology of the kidney and clinical indicators in patients with lupus nephritis (LN) using magnetic resonance imaging (MRI). METHODS: A total 50 female participants were enrolled in the study. Thirty patients with LN were divided into types 2, 3, 4, and 5, according to their pathological features. The control group consisted of 20 healthy female volunteers. Serum creatinine, C3, C1q, and anti-ds-DNA were measured. Conventional MRI, DTI, DWI, and BOLD scanning was performed to obtain the FA, ADC, and R2* values for the kidney. RESULTS: Compared with the control group, FA and the ADC were decreased in patients with LN, while the R2* value was increased (P < 0.05). The overall comparison of the SLEDAI (Activity index of systemic lupus erythematosus) score, total pathological score, AI, and serum creatinine C3 showed that these were significantly different between the two groups (P < 0.05). FA and the ADC were negatively correlated with urinary, blood ds-DNA, and serum creatinine and positively correlated with C1q (P < 0.05). The R2* value was positively correlated with urinary NGAL, blood ds-DNA, and serum creatinine (P < 0.05). FA and the ADC were negatively correlated with the SLEDAI score, total pathological score, AI, CI, nephridial tissue C3, and C1q. The R2* value was positively correlated with the SLEDAI score, total pathological score, AI, CI, nephridial tissue C3, and C1q (P < 0.05). CONCLUSIONS: MRI examination in female patients with LN was correlated with pathologic test results, which may have clinical significance in determining the disease's severity, treatment, and outcome.

OH-···Au Hydrogen Bond and Its Effect on the Oxygen Reduction Reaction on Au(100) in Alkaline Media.

Using ab initio molecular dynamics simulations with fully solvated ions, we demonstrate that solvated OH- forms a stable hydrogen bond with Au(100). Unlike the hydrogen bond between H2O and Au reported previously, which is more favorable for negatively charged Au, the OH-···Au interaction is stabilized when a small positive charge is added to the metal slab. For electro-catalysis, this means that while OH2···Au plays a significant role in the hydrogen evolution reaction, OH-···Au could be a significant factor in the oxygen reduction reaction in alkaline media. It also points to a fundamental difference in the mechanism of oxygen reduction between gold and platinum electrodes.

Ordered Intermetallic PtCu Catalysts Made from Pt@Cu Core/Shell Structures for Oxygen Reduction Reaction.

Platinum-based ordered intermetallic compounds are promising low-Pt catalysts toward the oxygen reduction reaction (ORR) for high-performance fuel cells. However, the synthesis of ordered intermetallic catalysts usually requires high-temperature annealing to overcome the energy barrier for atom diffusion, which leads to inevitable sintering of catalysts and greatly reduced mass-specific activity. Herein, we developed a new strategy to synthesize PtCu-ordered intermetallic catalysts by the generation of the Pt@Cu core/shell nanoparticles (Pt@Cu NPs) by Pt-assisted H2 reduction of Cu2+ with subsequent annealing at 500-1000 °C. Compared to the commonly used wet-impregnation method, the core/shell structure starts to form ordered PtCu alloys at a lower annealing temperature (500 °C). The Pt@Cu core/shell structure avoids the necessary process of Cu atoms diffusing to Pt NPs across the carbon supports occurred during high-temperature annealing in the wet-impregnation method, which ensures the formation of PtCu NPs with higher ordering degree while annealing at the same temperature. The highly ordered small-sized PtCu catalysts prepared by the core/shell strategy exhibit higher mass activity and specific activity compared to those prepared by the wet-impregnation method. Moreover, a positive correlation between the ORR activity and the ordering degree of the intermetallic PtCu NPs is identified, which could be associated with the increase of compressive strain with the ordering degree.

LncRNA GIHCG promoted the proliferation and migration of renal cell carcinoma through regulating miR-499a-5p/XIAP axis.

BACKGROUND: Our previous study demonstrated that lncRNA GIHCG is upregulated in renal cell carcinoma (RCC) and that knockdown of lncRNA GIHCG suppresses the proliferation and migration of RCC cells. However, the mechanism of lncRNA GIHCG in RCC needs further exploration. METHODS: The proliferation, cell cycle, migration, and apoptosis of RCC cells were tested using CCK-8, flow cytometry, wound healing and Annexin-V/-FITC/PI flow cytometry assays, respectively. Dual-luciferase reporter and RNA pull-down or RNA immunoprecipitation assays (RIPs) were performed to analyze the interactions among lncRNA GIHCG, miR-499a-5p and XIAP. A tumour xenograft study was conducted to verify the function of lncRNA GIHCG in RCC development in vivo. RESULTS: Knockdown of lncRNA GIHCG inhibited cell proliferation and migration and induced G0/G1 arrest while promoting apoptosis. Overexpression of lncRNA GIHCG led to the opposite results. LncRNA GIHCG sponged miR-499a-5p and downregulated its expression in RCC cells. MiR-499a-5p overexpression suppressed RCC cell growth. MiR-499a-5p targeted XIAP and inhibited its expression. LncRNA GIHCG knockdown reduced the growth of tumour xenografts in vivo and the expression of XIAP while increasing miR-499a-5p levels. CONCLUSION: LncRNA GIHCG accelerated the development of RCC by targeting miR-499a-5p and increasing XIAP levels.

Efficacy of Bushen Culuan decoction on ovarian follicle and follicular granulosa cells in mice with premature ovarian insufficiency induced by tripterygium wilfordii polyglycoside.

OBJECTIVE: To investigate the protective efficacy of Bushen Culuan decoction (BCD) on ovarian follicle and follicular granulosa cells in mice with premature ovarian insufficiency (POI) induced by tripterygium wilfordii polyglycoside, and to study the potential mechanism underlying the action. METHODS: Eighty female Balb/c mice were randomly divided into 4 groups (n = 20 each): blank group, model group, Bushen Culuan decoction intervening group (BCD group) and estradiol valerate intervening group (EV group). In the first 14 model establishing d, mice in model group, BCD group and EV group were under Tripterygium wilfordii polyglycoside (TWP) gavage to establish POI models. In the 14-day therapeutic stage, mice in BCD group were taken BCD 18.35 mg·kg-1d-1, mice in EV group were taken EV solution 0.15 mg·kg-1d-1, while mice in blank group and model group were taken normal saline. When the mice accomplished therapy, whole blood was collected for serum hormone including follicle stimulating hormone (FSH), luteal hormone (LH), estradiol (E2), antimullerian hormone (AMH) levels and vascular endothelial growth factor (VEGF), bone morphogenetic protein-7 (BMP-7) measurement. Ovarian tissues were harvested for morphologic observation, follicle counting, ovarian follicular graulosa cell apoptosis test and testing BMP-7 and caspase-3 expressions. RESULTS: The body weights of the mice kept growing stably in the process expect in TWP intervening stage. Compared with model group, BCD group had significantly higher ovarian index, serum E2, AMH, VEGF, BMP-7 levels and significantly lower FSH level (P < 0.05). Meanwhile the VEGF level in BCD group was higher than in EV group (P < 0.05). Compared with model group, the histopathological damage and GCs apoptosis were mitigated; developing follicle counting, BMP-7 expression were up-regulated, and caspase-3 expression was downregulated in BCD groups (P < 0.05). CONCLUSION: BCD treatment could attenuate pathological process in POI ovaries, suppress GC apoptosis, probably through promoting BMP-7 expression and following inhibiting caspase-3 activation.

circPlekha7 suppresses renal fibrosis via targeting miR-493-3p/KLF4.

Aims: The authors aim to investigate the function of circPlekha7 in renal fibrosis. Methods: Human renal tissues from chronic kidney disease patients, kidney cell line and primary cultured renal tubular epithelial cells were used. TGF-ß1-treated human kidney 2 cells/tubular epithelial cells and a unilateral ureteral obstruction mouse model were employed to study renal fibrosis. Results: circPlekha7 was diminished in renal tissues from chronic kidney disease patients and TGF-ß1-treated human kidney 2 cells and tubular epithelial cells, while miR-493-3p was upregulated. Overexpression of circPlekha7 or knockdown of miR-493-3p suppressed TGF-ß1 induced enhancements on epithelial to mesenchymal transition and fibrogenesis, as well as attenuated renal fibrosis and injury in mice subjected to unilateral ureteral obstruction. circPlekha7 bound with miR-493-3p, which directly targeted KLF4. Conclusion: circPlekha7 inhibits epithelial to mesenchymal transition of renal tubular epithelial cells and fibrosis via targeting miR-493-3p to de-repress KLF4/mitofusin2 expression.

Chronic kidney disease (CKD) ultimately leads to complete kidney dysfunction. The incidence of CKD continues to rise as a result of the increasingly aging population, and the treatment is very limited. In this study, the authors identified a novel molecule, circPlekha7, that plays a crucial role in CKD development and progression. The level of circPlekha7 is lower in the kidney tissues of CKD patients, and increasing its level could attenuate kidney injury and fibrosis. This work helps researchers understand the disease better and, more importantly, provides new avenues to develop therapy.

LncRNA Dlx6os1 Accelerates Diabetic Nephropathy Progression by Epigenetically Repressing SOX6 via Recruiting EZH2.

INTRODUCTION: Diabetic nephropathy (DN) is the leading cause of kidney failure worldwide. To explore the pathogenesis and effective biological target of DN is beneficial to seeking novel treatment strategies. OBJECTIVE: This study aimed to investigate the role of the lncRNA Dlx6os1/SOX6/EZH2 axis in DN progression. METHODS: PAS staining was performed to evaluate extracellular matrix accumulation; ELISA was carried out to assess the levels of urine microalbumin and blood glucose concentration; RT-qPCR was carried out to detect the levels of lncRNA Dlx6os1, TNF-α, IL-1ß, IL-6, SOX6, and EZH2. Western blot was performed to assess the levels of Col-IV, FN, TGF-ß1, and SOX6 proteins. RIP assay was carried out to verify the interaction between lncRNA Dlx6os1 and EZH2. ChIP-qPCR was conducted to verify the interaction between EZH2 and SOX6 promoter. RESULTS: Our results illustrated that lncRNA Dlx6os1 was highly expressed in DN mice and HG-induced SV40 MES13 cells. LncRNA Dlx6os1 knockdown inhibited HG-induced SV40 MES13 cell proliferation, fibrosis, and inflammatory cytokine release. LncRNA Dlx6os1 inhibited SOX6 expression by recruiting EZH2 in HG-SV40 MES13 cells, and SOX6 mediated the effects of lncRNA Dlx6os1 on proliferation, fibrosis, and inflammatory factor release of HG-induced SV40 MES13 cells. CONCLUSION: LncRNA Dlx6os1 accelerates the progression of DN by epigenetically repressing SOX6 via recruiting EZH2.

Catalysis of hydrogen evolution on Pt(111) by absorbed hydrogen.

The activity of Pt(111) electrodes for the hydrogen evolution reaction (HER) in 0.5M H2SO4 solution is found to increase with continuous potential cycling in the HER potential region. In addition, the basic cyclic voltammograms obtained in 0.5M H2SO4 saturated with N2 after HER show several characteristic changes: the current waves for hydrogen adsorption in the region of0.2 < E < 0.35 V and for sulfate adsorption at 0.35 < E < 0.5 V decrease and the current spike at 0.44 V for the phase transition of the sulfate adlayer gradually disappears. We suggest that these changes are caused by the absorption of a small amount of hydrogen in the subsurface layer and propose a mechanism by which this enhances hydrogen evolution.

[Examples of Professor MA Kun's treatment of infertility caused by hyperprolactinemia with kidney deficiency and blood stasis].

Hyperprolactinemia(HPRL) is one of the diseases leading to anovulatory infertility, which is a refractory gynecological disease and seriously affects female reproductive function. Professor MA Kun has summarized his experience in clinical and scientific studies for many years. And believes that kidney deficiency is the pathogenesis of HPRL and blood stasis is the dominant pathological manifestation of HPRL and can promote the progress of the disease. In view of this, Professor MA Kun took the therapy of kidney-tonifying and blood-activating as the principle for treating anovulatory infertility caused by HPRL, with soothing the liver and promoting Qi as adjuvant therapies. She has also summarized and refined the prescriptions for tonifying kidney and inducing ovulation, which have a remarkable clinical efficacy.

[Effect of therapies for kidney-tonifying and blood-activating in treatment of anovulatory infertility in eugenics].

In the context of the new era, paying attention to maternal and child health and advocating prenatal and postnatal care can effectively improve the quality of the birth population. Traditional Chinese medicine has a long history of prenatal and postnatal healthcare with rich content, which is the theoretical basis of modern related services. With the social development and the improvement of people's awareness of prenatal and postnatal healthcare, people have gradually shifted the focus of prenatal and postnatal healthcare to the peri-pregnancy stage at present, namely that couples of childbearing age are guided to prepare for pregnancy under the premise of solving their basic diseases. Infertility is a common and refractory disease for women of childbearing age. Ovulation disorder is one of its common pathological mechanisms. Traditional Chinese medicine believes that kidney deficiency is the main cause and pa-thogenesis of anovulation infertility and blood stasis is an important factor throughout the disease course. In clinical practice, therapies for invigorating kidney and activating blood are safe and reliable to treat anovulatory infertility mainly by adjusting the hypothalamus-pituitary-ovarian axis, improving ovarian function, uterine environment and gamete quality and increasing endometrial volume. Under the guidance of the thought of prenatal and postnatal healthcare, the authors tried to explore the effect of therapies for kidney-tonifying and blood-activating in the treatment of anovulatory infertility in eugenics, with the purpose of providing ideas and basis for subsequent relevant clinical studies and contributing to prenatal and postnatal healthcare services.

[Study on mechanism of Bushen Culuan Formula in treatment of polycystic ovary syndrome based on network pharmacology and molecular docking].

This study used network pharmacology and molecular docking to study the mechanism of Bushen Culuan Formula in the treatment of infertility caused by polycystic ovary syndrome(PCOS). The active ingredients and potential drug targets of Bushen Cu-luan Decoction were obtained by searching the Traditional Chinese Medicine System Pharmacology(TCMSP) database, and the targets of PCOS by searching GeneCards. After the drug targets and disease targets were corrected by Uniprot, the intersection genes were obtained. STRING database and Cytoscape 3.7.2 were used for protein-protein interaction(PPI) analysis of the intersection genes. The ClueGO plug-in of Cytoscape 3.7.2 was employed to perform gene ontology(GO) enrichment and KEGG pathway enrichment for the intersection genes. Finally, molecular docking of the key active ingredients with the targets of Bushen Culuan Formula was performed using AutoDockVina and MGLtools. A total of 136 active ingredients and 314 drug targets of the decoction were obtained from TCMSP, and 136 disease targets from GeneCards. Finally, 49 drug-disease intersection genes were obtained. GO enrichment found that the genes were mainly involved in the regulation of muscle cell apoptosis, positive regulation of small molecule metabolism, core promoter binding, RNA polymerase Ⅱ regulation of pri-miRNA transcription, negative regulation of transmembrane transport and other biological functions. The enriched KEGG pathways mainly included MAPK, PI3 K-Akt, p53, and HIF-1 signaling pathways. The results of molecular docking showed that quercetin and PTGS2 can bind stably and interact through amino acid residues THR206, TRP387, ASN382, etc. This study preliminarily reveals the multi-component, multi-target, and multi-pathway mechanism of Bushen Culuan Formula in the treatment of PCOS-related infertility, which provides a basis for further research.