Impact of Regional Collaborative Network on the Rescue of Patients with ST-Elevation Myocardial Infarction First Visit to non-PCI Hospitals.

Objective: To assess the effect of a regional collaborative network on the treatment of ST-elevation myocardial infarction (STEMI) patients first admitted to non- percutaneous coronary intervention (PCI) hospitals. Methods: Using data from Kunshan Hospital of Traditional Chinese Medicine's chest pain center database, patients were grouped based on the establishment of the regional collaborative rescue network. Key timepoints and in-hospital complications were analyzed. Results: A total of 152 ST-elevation myocardial infarction patients were included in the study. Compared to control group, symptom-to-balloon time (S-B), time of first medical contact to balloon and inter-hospital referral time in observation group were significantly shorter [(314.03 ± 209.26) min vs (451.27 ± 290.44) min, P = .001], [(115.32 ± 54.73) min vs (191.67 ± 130.30) min, P = .001], [(55.09 ± 37.23) min vs (112.67 ± 95.90) min, P = .001], but time of symptom to first medical contact were not statistically significant[(210.27±217.07) min vs (239.61 ± 200.92) min, P = .136].The incidence of heart failure and total complications during hospitalization decreased [7 (8.14%) vs 13 (19.70%), P = .037] and [14 (16.28%) vs 24 (36.36%), P = .004]. However no statistically significant difference were observed in rate of death during hospitalization [2 (2.33%) vs 3 (4.55%), P = .450], ventricular fibrillation [2 (2.33%) vs 3 (4.55%), P = .450], left ventricular thrombosis [2 (2.33%) vs 4 (6.06%), P = .244] and recurrent myocardial infarction[1 (1.16%) vs 1 (1.52%), P = .851]. Conclusions: The regional cooperative rescue network notably reduces ischemic and referral times for STEMI patients, lowering the incidence of heart failure during their hospital stay.

Folic Acid Protects Against Kidney Damage in Mice with Diabetic Nephropathy by Inhibiting M1 Macrophage Polarization via Nuclear Factor-k-gene Binding Pathway.

Kidney damage is one of the most common complications of diabetes, and inflammation caused by macrophage infiltration plays an important role. Folic acid (FA), a water-soluble vitamin, was previously found to affect inflammation by regulating macrophage polarization. In our study, we aimed to investigate the effect of FA on renal injury in mice with diabetic nephropathy (DN). We found that FA treatment ameliorated diabetic metabolic parameters in mice with DN, including reducing 24-hour food consumption, 24-hour urine volume and 24-hour water intake and increasing body weight and serum insulin. Of note, FA treatment improved renal functional and structural damage in mice with DN. In addition, FA treatment significantly reduced the number of renal infiltrating M1 macrophages, inflammatory cytokine FA stimulation significantly reduced the increase in F4/80+CD86+ cell ratio, inflammatory factor content and p-p65/p65 protein expression induced by high glucose exposure in RAW264.7 cells. All in all, our results indicated that FA protects against kidney damage in mice with DN by inhibiting M1 macrophage polarization, and its mechanism may be related to the inhibition of nuclear factor-k-gene binding (NF-kB) signaling pathway.

MicroRNA­21 contributes to the puerarin­induced cardioprotection via suppression of apoptosis and oxidative stress in a cell model of ischemia/reperfusion injury.

Puerarin, a major bioactive constituent of the Radix puerariae, can ameliorate myocardial ischemia/reperfusion (I/R) injury. Emerging evidence supports that microRNA (miR)­21 functions as a protective factor against I/R and/or hypoxia­reperfusion (H/R)­induced myocardial injury. However, the role of miR­21 in the cardioprotective effect of puerarin remains unclear. Therefore, the purpose of the present study was to demonstrate the involvement of miR­21 in the cardioprotective mechanisms of puerarin using a cell model of I/R injury, generated by culturing rat H9c2 cardiomyocytes under H/R conditions. The results demonstrated that pre­treatment with puerarin significantly increased cell viability, decreased lactate dehydrogenase activity and upregulated miR­21 expression in H/R­treated H9c2 cells. Transfection of an miR­21 inhibitor led to an increase in H/R­induced cytotoxicity and reversed the protective effects of puerarin. Additionally, miR­21 inhibition attenuated the puerarin­induced decrease in the rate of apoptosis, caspase­3 activity and the expression of apoptosis regulator Bax, and increased apoptosis regulator Bcl­2 expression, under H/R conditions. Furthermore, puerarin mitigated H/R­induced oxidative stress as evidenced by the decrease in endogenous reactive oxygen species production, malondialdehyde content and NADPH oxidase 2 expression, and enhanced the antioxidative defense system as illustrated by the increase in superoxide dismutase activity, catalase and glutathione peroxidase levels. These effects were all eliminated by miR­21 inhibitor transfection. Furthermore, the miR­21 inhibitor exacerbated the H/R­induced oxidative stress and attenuated the antioxidative defense system in H/R­treated H9c2 cells. Taken together, the results suggested that miR­21 mediated the cardioprotective effects of puerarin against myocardial H/R injury by inhibiting apoptosis and oxidative stress.