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Background: Currently, there are many different drugs to improve Alzheimer’s disease (AD) from different pathways. As a supplement and alternative medicine, traditional Chinese medicine (TCM) targets multiple pathways which may be different from classical Western medicine, which may be orchestrated with Western medicine to materialize multiplying efficacy in AD patients.Objective: To investigate the therapeutic effect and assess the available preclinical evidence and possible mechanisms of β-asarone which was extracted from Acorus gramineus Soland (Araceae, AGS) for AD based on rat and mouse animal models.Methods: PubMed, Embase, Scopus, Cochrane Library, BIOSIS Previews, Web of Science, EBSCO, and Google Scholar were searched from inception to 5 May 2022. Rat and mouse experiments assessing the therapeutic effects of β-asarone for AD were included. Primary outcomes were neuroethology, including escape latency and times of crossing platform. Second outcomes were cell apoptosis, including Bax and Bcl-2. The weighted mean difference (WMD) was generated for continuous variables. The relative outcomes were analyzed with the aid of Get Data Graph Digitizer 2.26 and software STATA version 16.0 MP.Results: For the primary endpoint, compared with the modeling group, β-asarone significantly decreased the escape latency (WMD = -12.61, 95% CI: -18.66 to -6.57) and increased the times of crossing platform (WMD = 1.50, 95% CI: 0.31–2.70). For the secondary endpoint, β-asarone remarkably reduced the relative expression of the amyloid precursor protein (APP) (WMD = −2.25, 95% CI: −2.49 to −2.01), decreased the expression of the apoptosis-related protein, associated X protein (Bax) (WMD = −2.40, 95% CI: −3.51 to −1.29), lowered the expression of apoptosis-related protein, B-cell lymphoma-2 (Bcl-2) (WMD = 0.42, 95% CI: 0.38–0.46), and decreased the signal pathway-related proteins, phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) (WMD = −0.70, 95% CI: −0.93 to −0.47) over the control group.Conclusion: β-asarone spectacularly improved the learning ability and memory in rats and mice, which might be correlated with its potential neuroprotective effect through multiple signaling pathways.

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Introduction Ventricular septal rupture is an important high-mortality complication in the scope of myocardial infarctions. The effectiveness of different treatment modalities is still controversial. This meta-analysis compares the efficacy of percutaneous closure vs. surgical repair for the treatment of postinfarction ventricular septal rupture (PI-VSR). Methods A meta-analysis was performed on relevant studies found through PubMed®, Embase, Web of Science, Cochrane Library, China National Knowledge Infrastructure (or CNKI), Wanfang Data, and VIP databases searching. The primary outcome was a comparison of in-hospital mortality between the two treatments, and the secondary outcome was documentation of one-year mortality, postoperative residual shunts, and postoperative cardiac function. Differences were expressed as odds ratios (ORs) with 95% confidence intervals (CIs) to assess the relationships between predefined surgical variables and clinical outcomes. Results Qualified studies (742 patients from 12 trials) were found and investigated for this meta-analysis (459 patients in the surgical repair group, 283 patients in the percutaneous closure group). When comparing surgical repair to percutaneous closure, it was found that the former significantly reduced in-hospital mortality (OR: 0.67, 95% CI 0.48-0.96, P=0.03) and postoperative residual shunts (OR: 0.03, 95% CI 0.01-0.10, P<0.00001). Surgical repair also improved postoperative cardiac function overall (OR: 3.89, 95% CI 1.10-13.74, P=0.04). However, there was no statistically significant difference in one-year mortality between the two surgical strategies (OR: 0.58, 95% CI 0.24-1.39, P=0.23). Conclusion We found that surgical repair appears to be a more effective therapeutic option than percutaneous closure for PI-VSR.

Salvia miltiorrhiza (SAL) and Panax notoginseng (PNS) is widely used for the treatment of ischemic stroke. However, what components of SAL and PNS protect brain microvascular pericytes after ischemic stroke remains unclear. We evaluated protective effects and mechanisms of the components of SAL and PNS in pericytes subjected to oxygen-glucose deprivation /reoxygenation (OGD/R). Pericytes were subjected to OGD/R. Cell Counting Kit-8 (CCK-8) was performed to evaluate cell viability. ROS and SOD kits were performed to detect oxidative stress. Flow cytometry was performed to analyze cells apoptosis. Scratch assay was performed to evaluate cells migration. Western blot was performed to detected expression of apoptosis proteins, VEGF, Ang-1, PDGFRβ, PI3K/AKT and JNK/ERK/P38 signaling pathways. Results showed Salvianolic acid B (Sal B), Salvianolic acid B (Sal D), Notoginsenoside R1(R1), Ginsenoside Rb1 (Rb1) and Ginsenoside Rg1 (Rg1) increased cell viability of pericytes subjected to OGD/R, reduced the level of ROS and increased the expression of SOD. The components reduced cells apoptosis, increased the proteins level of Bcl-2/Bax, reduced the level of Cleaved caspased3/caspase3, increased cells migration and enhanced the levels of Ang-1, PDGFR-β and VEGF. The components could activate PI3K/AKT/mTOR pathway, inhibit JNK/ERK/P38 pathway. Studies found that Sal B, Sal D, R1, Rb1 and Rg1 inhibited oxidative stress and apoptosis, increased release of pro-angiogenic regulators of pericytes-related to PI3K/AKT/mTOR and JNK/ERK/P38 signaling pathways. This provides a candidate basis for the development of monomeric drugs for treatment of ischemic stroke.