Vascular dementia (VaD) is the second most prevalent dementia, which is attributable to neurovascular dysfunction. Currently, no approved pharmaceuticals are available. Taohong Siwu decoction (TSD) is a traditional Chinese medicine prescription with powerful antiapoptosis and anti-inflammatory properties. In this study, a network pharmacology approach together with molecular docking validation was used to explore the probable mechanism of action of TSD against VaD. A total of 44 active components, 202 potential targets of components, and 3,613 VaD-related targets including 161 intersecting were obtained. The potential chemical components including kaempferol, baicalein, beta-carotene, luteolin, quercetin, and beta-sitosterol involved in the inflammatory response, oxidative stress, and apoptosis might have potential therapeutic effects on the treatment of VaD. The potential core targets including AKT1, CASP3, IL1β, JUN, and TP53 associated with cell apoptosis and inflammatory might account for the essential therapeutic effects of TSD in VaD. The results indicated that TSD protected against VaD through multicomponent and multitarget modes. Though the detailed mechanism of action of various active ingredients needs to be further illustrated, TSD still showed a promising therapeutic agent for VaD due to its biological activity.
Estrogen receptor is involved in the pathogenesis of recurrent spontaneous abortion (RSA). The ESR1 and ESR2 genes can mediate nongenomic estrogen responses. This study aimed to assess the genetic association between the ESR1 and ESR2 genes polymorphisms and RSA susceptibility in a Chinese Han population. A total of 258 women who had experienced RSA and 264 unrelated healthy women were recruited. Genotypes of the 6 polymorphisms in the ESR1 (rs9340799, rs2234693, and rs3798759) and ESR2 genes (rs207764, rs4986938, and rs1256049) were analyzed using Snapshot technology. No association was detected between the alleles and genotypes of ESR1 rs9340799, rs2234693, and rs3798759 polymorphims and RSA risk (P > .05). Subjects carrying the haplotype of rs9340799A-rs2234693C-rs3798759A had a significantly increased RSA risk in the case group compared with the control group (P = .0005, P adj = .003, odds ratios [95% CI] = 0.35 [0.19-0.65]). However, subjects carrying the haplotype of rs9340799G-rs2234693C-rs3798759A had a significantly decreased RSA risk in the case group compared with the control group (P = .0005, P adj = .003, odds ratios [95% CI] = 2.99 [1.57-5.70]). In addition, no association was found between the alleles, genotypes, and haplotypes of ESR2 rs207764, rs4986938, rs1256049 polymorphisms and RSA risk (P > .05). In conclusion, the haplotype rs9340799A-rs2234693C-rs3798759A of ESR1 might be a risk factor. And the haplotype rs9340799G-rs2234693C-rs3798759A of ESR1 might be a protective factor for RSA in a Chinese Han population.
INSR and ISR-1 may be candidate genes for essential hypertension (EH). However, the genetic association between the INSR and ISR-1 gene polymorphisms and EH risk remains contradictory. To determine a more precise association of the INSR and ISR-1 gene polymorphisms and EH, the present study performed a meta-analysis. Eligible studies up to Jan 2021 were retrieved from multiple databases including PubMed, Embase, Web of Science and China National Knowledge Infrastructure. The pooled odds ratio (OR) and 95% confidence interval (CI) were used to evaluate the genetic associations between the allele, dominant and recessive models of INSR Nsil, RsaI and ISR-1 G972R polymorphisms and EH susceptibility. A total of 10 case-control studies encompassing 2,782 subjects including 1,289 cases and 1,493 controls were evaluated for the present meta-analysis. Neither of the allele, dominant and recessive models of INSR Nsil and ISR-1 G972R polymorphisms was associated with EH risk (P>0.05). While the allele [P=0.0008, OR=0.58, (95% CI)=(0.42, 0.80)], dominant [P=0.02, OR=0.59, (95% CI)=(0.38, 0.92)] and recessive models [P=0.003, OR=0.38, (95% CI)=(0.20, 0.72)] of INSR Rsal polymorphism were associated with decreased risk of EH. Subgroup analysis according to ethnicity showed that the significant associations between the allele, dominant and recessive models of INSR Rsal polymorphism and EH risk were observed in Caucasian populations, but not in Asian populations (P>0.05). In conclusion, the INSR Rsal polymorphism is probably a protective factor for EH. To identify the result, additional case-control designed research with larger numbers of subjects are required.
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