Objective:To systematically evaluate the correlation between chronic non-occupational arsenic exposure and hypertension.Methods:A literature search was conducted through Web of Science, Pubmed, Embase, Cochrane Library, WanFang Data, China National Knowledge Infrastructure (CNKI), VIP Chinese Journal Service Platform (VIP) Database and China Biomedical Literature Database to comprehensively collect epidemiological literature related to chronic non-occupational arsenic exposure and hypertension published domestically and internationally for inclusion in the study, with a time limit from database establishment to January 1, 2023. Meta-analysis of dichotomous variables was conducted using Stata MP15 software, with odds ratio ( OR) value [95%confidence interval( CI)] as the effect evaluation indicator. A random-effects model or a fixed-effects model was selected for comprehensive quantitative analysis according to the heterogeneity results; the sources of heterogeneity were identified through subgroup analysis; a funnel plot was used for qualitative analysis of publication bias and the results were further assessed by Egger test. Stata 15.0 software was then used to analyze the dose-response relationship between chronic non-occupational arsenic exposure and hypertension using restricted cubic spline function and generalized least squares estimation (GLST) method. Results:Twenty-nine articles ( n = 127 258) were finally included, including 24 English articles and 5 Chinese articles. Through Meta-analysis, the combined OR value (95% CI) for hypertension was 1.07 (1.04 - 1.09), with a statistically significant difference ( P < 0.05). The combined OR values (95% CI) for urinary arsenic, drinking water arsenic, and hair arsenic in subgroup analysis were 1.10 (1.04 - 1.17), 1.13 (1.07 - 1.20), and 2.55 (1.55 - 4.20), respectively. The combined OR values (95% CI) for cross-sectional studies, case-control studies and cohort studies were 1.11 (1.06 - 1.16), 1.13 (1.04 - 1.23) and 1.04 (1.00 - 1.07), respectively. For every unit (μg/L) increase in arsenic exposure in drinking water, the risk of hypertension increased by 0.13% [ OR value (95% CI): 1.001 269 (1.000 104 - 1.002 434), P < 0.05]. Conclusions:There is a correlation between chronic non-occupational arsenic exposure and adult hypertension, with urinary arsenic, drinking water arsenic and hair arsenic as possible exposure markers. There is a non-linear dose-response relationship between chronic non-occupational arsenic exposure and adult hypertension.

Blood deficiency syndrome (BDS) refers to a pathological state with blood dysfunction and organ dystrophy in traditional Chinese medicine. Danggui Wuji granules (DWG) was developed from a formula containing Angelicae Sinensis Radix and Musculus et Os Galli Domestici. Herein, we investigated the mechanism of DWG in treating BDS by modulating gut microbiota. We found that DWG protected mice from BDS by elevating the levels of red blood cell count, hemoglobin, and hematocrit in peripheral blood and increasing the erythrocyte membrane Na⁺-K⁺-ATPase activity. Danggui Wuji granules changed the composition and metabolites of colonic flora. Notably, Lactobacillus, Muribaculaceae, and Alistipes were the main genera showing changes after DWG treatment. Our findings revealed that DWG presented a positive therapeutic effect on BDS in mice by regulating the gut microbiota and metabolites. The protective mechanism of DWG was associated with pathways such as metabolic pathways, biosynthesis of secondary metabolites, ABC transporters, ribosome, thyroid hormone synthesis, lysine degradation, galactose metabolism, tyrosine metabolism, etc.

ObjectiveTo clarify the therapeutic effect of Huashi Baidu prescription on pneumonia in mice caused by influenza A （H1N1） virus and explore its mechanism based on the transcriptome. MethodA mouse influenza viral pneumonia model was built by intranasal infection with influenza A virus， and mice were continuously administered the drug for five days， so as to investigate the general condition， lung index， viral load， pathological morphology of lung tissue， survival time， and prolongation rate of survival time of mice and clarify the therapeutic effect of Huashi Baidu prescription on influenza viral pneumonia. Transcriptome technology was used to detect the differentially expressed genes in the lung tissue of mice in the model group and the normal group， as well as the Huashi Baidu prescription group and the model group， and the potential core target of the Huashi Baidu prescription for the treatment of influenza viral pneumonia was screened. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to verify the effect of Huashi Baidu prescription on the mRNA expression level of core target genes. ResultCompared with the normal group， the lung index and viral load in the lung tissue of the model group were significantly increased （P<0.05， P<0.01）. Compared with the model group， the high-dose group of Huashi Baidu prescription significantly prolonged the survival time of mice infected with influenza A virus （P<0.05） and significantly reduced the lung index value of mice （P<0.05） and the viral load of lung tissue. The high-dose， medium-dose， and low-dose groups of Huashi Baidu prescription could significantly reduce lung tissue inflammation， blood stasis， swelling， and other pathological changes in mice （P<0.05， P<0.01）. Transcriptome analysis of lung tissue showed that core genes were mainly enriched in the nuclear transcription factor-κB （NF-κB） signaling pathway， interleukin-17 （IL-17） signaling pathway， cytokine-cytokine receptor interaction， and other pathways after the intervention of Huashi Baidu prescription. TRAF6， NFKBIA， CCL2， CCL7， and CXCL2 were the top five node genes with combined score values. Real-time PCR validation showed that Huashi Baidu prescription significantly downregulated the mRNA expression of key genes TRAF6 and NFKBIA in the NF-κB signaling pathway， as well as chemokines CCL2， CCL7， and CXCL2 （P<0.05， P<0.01）. ConclusionHuashi Baidu prescription has a therapeutic effect on influenza viral pneumonia， possibly by inhibiting the expression of key nodes TRAF6 and NFKBIA in the NF-κB signaling pathway and that of chemokines CCL2， CCL7， and CXCL2， reducing the recruitment of inflammatory cells and viral load， and exerting anti-influenza viral pneumonia effects.