The effect of gum consumption on blood pressure as a risk factor for coronary heart disease: A meta-analysis of controlled trials.

Guar gum has been used in the management of hypercholesterolemia, constipation, weight loss, type 2 diabetes mellitus and hypertension. Our aim was to verify the hypothesis that Guar gum can be used as an alternative to pharmacological agents in the treatment of mild hypertension. Thus, we conducted a systematic review and meta-analysis to evaluate the effectiveness of Guar gum in reducing blood pressure. We searched the Cochrane Library, PubMed/Medline, Scopus and Google Scholar databases for studies published in the English language up to June 2020 which evaluated the effects of gum consumption on systolic blood pressure (SBP) and diastolic blood pressure (DBP). Nine randomized clinical trials with suitable comparison groups (placebo/control) reported SBP and DBP as outcome measures. These trials involved in total 640 participants. The overall results indicated that the consumption of gum resulted in a significant change in SBP (WMD: -1.190 mmHg, 95% CI: -2.011, -0.370) and DBP (WMD: -1.101 mmHg, 95% CI: -1.597, -0.605). Moreover, the greatest reduction in blood pressure was seen in patients with type 2 diabetes mellitus and metabolic syndrome who consumed Guar gum (WMD: -3.375 mmHg). In addition, there was a significant decrease in SBP if the gum dosage was > 15 g (WMD: -6.637 mmHg) and if the intervention duration was > 12 weeks (WMD: -1.668 mmHg). The results of the present dose-response meta-analysis support the employment of gum consumption in the reduction of SBP and DBP. Based on the sub-group analyses, we highlight that the greatest decrease in SBP was experienced if the gum dosage was > 15 g and when the intervention lasted > 12 weeks.

Selenium donor restricts the intracellular growth of Mycobacterium tuberculosis through the induction of c-Jun-mediated both canonical autophagy and LC3-associated phagocytosis of alveolar macrophages.

The relationship between selenium and Mycobacterium tuberculosis (MTB) infection has been reported previously; however, the specific mechanism is still not clear. In this study, selenium levels decreased in the serum of patients with pulmonary tuberculosis (PTB) compared with the healthy controls; they were associated with the treatment outcome of such patients. The qRT-PCR assay revealed that selenium might function through proinflammatory and autophagy pathways. The treatment with methylseleninic acid (MSeA), a selenium donor, blocked the M1 polarization of MTB-infected macrophages through the induction of both canonical autophagy and LC3-associated phagocytosis (LAP). c-Jun is vital in mediating the MSeA-triggered canonical autophagy and LAP process, thus displaying a restricting function against intracellular MTB. An in vivo study confirmed that the activity of MSeA was shown through enhancing macrophage autophagy related pathway. The results showed that selenium had a restricting function against intracellular MTB by regulating autophagy in macrophages. The findings might provide a novel direction for PTB therapy in the future.

Histone deacetylase 9-mediated phenotypic transformation of vascular smooth muscle cells is a potential target for treating aortic aneurysm/dissection.

Aortic aneurysm/dissection (AAD) is a serious cardiovascular condition characterized by rapid onset and high mortality rates. Currently, no effective drug treatment options are known for AAD. AAD pathogenesis is associated with the phenotypic transformation and abnormal proliferation of vascular smooth muscle cells (VSMCs). However, endogenous factors that contribute to AAD progression remain unclear. We aimed to investigate the role of histone deacetylase 9 (HDAC9) in AAD pathogenesis. HDAC9 expression was considerably increased in human thoracic aortic dissection specimens. Using RNA-sequencing (RNA-seq) and chromatin immunoprecipitation, we demonstrated that HDAC9 transcriptionally inhibited the expression of superoxide dismutase 2 and insulin-like growth factor-binding protein-3, which are critically involved in various signaling pathways. Furthermore, HDAC9 triggered the transformation of VSMCs from a systolic to synthetic phenotype, increasing their proliferation and migration abilities and suppressing their apoptosis. Consistent with these results, in vivo experiments revealed that TMP195, a pharmacological inhibitor of HDAC9, suppressed the formation of the ß-aminopropionitrile-induced AAD phenotype in mice. Our findings indicate that HDAC9 may be a novel endogenous risk factor that promotes the onset of AAD by mediating the phenotypic transformation of VSMCs. Therefore, HDAC9 may serve as a potential therapeutic target for drug-based AAD treatment. Furthermore, TMP195 holds potential as a therapeutic agent for AAD treatment.

Influence of sex and menopausal status on the relationship between metabolic syndrome and coronary artery calcification: a Chinese community-based cross-sectional study.

OBJECTIVE: To evaluate the association between metabolic syndrome and coronary artery calcification according to different sex and menopausal status. METHODS: This cross-sectional study included 2,704 adults from the Jidong community (Tangshan, China) recruited from July 2013 to August 2014. Adults aged ≥40 years with no cardiovascular disease and with coronary artery calcification score data were included. Metabolic syndrome was defined according to the 2005 International Diabetes Federation standard. Coronary artery calcification score was determined using the Agatston method. The associations between metabolic syndrome and coronary artery calcification prevalence were evaluated using logistic regression. RESULTS: In the multivariable regression analysis, metabolic syndrome was associated with coronary artery calcification (odds ratio: 1.34, 95% confidence interval: 1.04-1.71, P = 0.021). When stratified by sex, metabolic syndrome was positively associated with coronary artery calcification prevalence in female participants (odds ratio: 2.79, 95% confidence interval: 1.96-3.96, P < 0.001), whereas no association was observed in male participants. Furthermore, metabolic syndrome was associated with a higher prevalence of coronary artery calcification (P < 0.001) independent of adjustment for covariates in postmenopausal women than in premenopausal women, and coronary artery calcification prevalence increased with an increase in conditions related to metabolic syndrome. CONCLUSIONS: Our findings indicate that metabolic syndrome in postmenopausal women is associated with a higher prevalence of coronary artery disease than in premenopausal women and men.