Myocardial ischemia‑reperfusion injury is one of the most common cardiovascular diseases, and can lead to serious damage and dysfunction of the myocardial tissue. Previous studies have demonstrated that berberine exhibits ameliorative effects on cardiovascular disease. The present study further investigated the efficacy and potential mechanism underlying the effects of berberine on ischemia‑reperfusion injury in a mouse model. Inflammatory markers were measured in the serum and levels of inflammatory proteins in myocardial cells were investigated after treatment with berberine. In addition, the apoptosis of myocardial cells was investigated after berberine treatment. Apoptosis‑associated gene expression levels and apoptotic signaling pathways were analyzed in myocardial cells after treatment with berberine. The phosphoinositide 3‑kinase (PI3K)/RAC‑α serine/threonine‑protein kinase (AKT) and nuclear factor (NF)‑κB signaling pathways were also analyzed in myocardial cells after treatment with berberine. Histological analysis was used to analyze the potential benefits of berberine in ischemia‑reperfusion injury. The present study identified that inflammatory responses and inflammatory factors were decreased in the myocardial cells of the mouse model of ischemia‑reperfusion injury. Mechanism analysis demonstrated that berberine inhibited apoptotic protease‑activating factor 1, caspase‑3 and caspase‑9 expression in myocardial cells. The expression of Bcl2‑associated agonist of cell death, Bcl‑2‑like protein 1 and cellular tumor antigen p53 was upregulated. Expression of NF‑κB p65, inhibitor of NF‑κB kinase subunit β (IKK‑β), NF‑κB inhibitor α (IκBα), and NF‑κB activity, were inhibited in myocardial cells in the mouse model of ischemia‑reperfusion injury. In conclusion, the results of the present study indicate that berberine inhibits inflammatory responses through the NF‑κB signaling pathway and suppresses the apoptosis of myocardial cells via the PI3K/AKT signaling pathway in a mouse model of ischemia‑reperfusion injury. These results suggest that berberine is a potential drug for the treatment of patients with ischemia‑reperfusion injury.

Background. Huangqi Gegen decoction (HGD), a Chinese herb formula, has been widely used to treat diabetic nephropathy in China, while the pharmacological mechanisms are still unclear. Therefore, the present study aims to explore the underlying mechanism of HGD for treating diabetic nephropathy (DN). Materials and Methods. Traditional Chinese Medicine Systems Pharmacology Database (TCMSP), UniProt, and SwissTargetPrediction databases were used to search the active ingredients and potential targets of HGD. In addition, multiple disease-related databases were used to collect DN-related targets. Common targets of the protein-protein interaction (PPI) network were established using the STRING database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the DAVID database. At last, AutoDockVina was used to conduct molecular docking verification for the core components and targets. Results. A total of 27 active ingredients and 354 putative identified target genes were screened from HGD, of which 99 overlapped with the targets of DN and were considered potential therapeutic targets. Further analysis showed that the HGD activity of quercetin, formononetin, kaempferol, isorhamnetin, and beta-sitosterol ingredients is possible through VEGFA, IL6, TNF, AKT1, and TP53 targets involved in TNF, toll-like receptors, and MAPK-related pathways, which have anti-inflammatory, antiapoptosis, antioxidation, and autophagy effects, relieve renal fibrosis and renal cortex injury, and improve renal function, thus delaying the development of DN. The molecular docking results showed that quercetin, formononetin, kaempferol, isorhamnetin, beta-sitosterol had a good binding activity with VEGFA, IL6, TNF, AKT1, and TP53. Conclusion. This study demonstrated that HGD might take part in the treatment of DN through multicomponent, multitarget, and multichannel combined action.

Purpose To report endovascular repair with the chimney technique of type B aortic dissection involving a right-sided aortic arch (RAA). Case Reports Two hypertensive men aged 48 and 42 years with symptoms of aortic dissection resistant to medical therapy underwent emergent thoracic endovascular aortic repair with the chimney technique to extend the proximal landing zones. Both patients had right-sided arches with mirror image branching. One patient required a bare metal chimney stent to maintain perfusion to the right subclavian artery, while the other patient had a chimney stent to revascularize the right common carotid artery. Short-term follow-up (1 year and 1 month, respectively) showed that there was positive aortic remodeling, and the chimney stents were patent. Conclusion Chimney TEVAR seems safe and effective for Stanford type B dissection in patients having RAA with mirror image branching and no sufficient proximal fixation zone.

Summary: Aims: 2‐(4‐methyl‐thiazol‐5‐yl) ethyl nitrate maleate (NMZM), a derivative of clomethiazole (CMZ), had been investigated for the treatment of Alzheimer's disease (AD). The beneficial effects of NMZM in AD included reversing cognitive deficit, improving learning and memory as well as neuroprotection. The pharmacological effects of NMZM on GABA_Areceptors were reported previously; however, the mechanisms were unclear and were explored therefore.Results: In this study, we demonstrated that NMZM improved learning and memory by alleviating scopolamine‐induced long‐term potentiation (LTP) suppression in the dentate gyrus of rats, indicating that NMZM had protective effects against scopolamine‐induced depression of LTP. Next, we investigated the action of NMZM on GABA_Areceptors in hippocampal neurons and the binding site of NMZM on GABA_Areceptors. NMZM directly activated GABA_Areceptors in hippocampal neurons in a weak manner. However, NMZM could potentiate the response of GABA_Areceptors to GABA and NMZM positively modulated GABA_Areceptors with an EC₅₀value of 465 μmol/L at 3 μmol/L GABA while this potentiation at low concentration of GABA (1, 3 μmol/L) was more significant than that at high concentration (10, 30 μmol/L). In addition, NMZM could enhance GABA currents after using diazepam and pentobarbital, the positive modulators of GABA_Areceptors. NMZM could not affect the etomidate‐potentiated GABA_Acurrent. It suggested that the binding site of NMZM on GABA_Areceptors is the same as etomidate.Conclusions: These results provided support for the neuroprotective effect of NMZM, which was partly dependent on the potentiation of GABA_Areceptors. The etomidate binding site might be a new target for neuronal protection and for drug development.