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Objective: To explore the efficacy of voriconazole combined with glucocorticoid on the nephrotic syndrome in children., Patients and Methods: A total of 62 children with nephrotic syndrome were enrolled in this study. They were treated in our hospital from February 2016 to August 2019, including 35 children treated with voriconazole in a control group, and 27 children treated with glucocorticoid combined with voriconazole in a research group. The efficacy was evaluated, and a logistic regression analysis was carried out to find out the risk factors affecting the efficacy. The enzyme-linked immunosorbent assay (ELISA) was used to determine the serum creatinine and urine protein expression before and after treatment. In addition, receiver operating characteristic (ROC) curves were drawn to analyze the predictive value of serum creatinine and urine protein expression., Results: The marked efficacy and total effective rate in the research group were significantly higher than those in the control group, while the non-efficacy in the research group was significantly lower than that in the control group (p<0.05). After treatment, the expression of serum creatinine and urine protein in the research group was significantly lower than that in the control group (p<0.05). The area under the curve (AUC) of urine protein was 0.798. The AUC of serum creatinine was 0.724. Multivariate logistic regression analysis revealed that serum albumin, high edema, infection, serum creatinine, and urine protein were independent risk factors., Conclusions: Glucocorticoid can improve clinical efficacy. Serum creatinine and urine protein can be adopted as predictive factors for efficacy on children with nephrotic syndrome. Serum albumin, high edema, infection, serum creatinine, and urine protein were independent risk factors for the efficacy on children with nephrotic syndrome.

Objective: Ischemic postconditioning (IPO) reduces lethal reperfusion injury under normal conditions, but its effectiveness is blocked by hypercholesterolemia (HC). This study aims to determine whether blocking the mitochondrial permeability transition pore (mPTP) with cyclosporine-A (CsA) can restore cardioprotection of IPO in hypercholesterolemic rat heart., Materials and Methods: Isolated rat hearts underwent 30 min global ischemia and 120 min reperfusion. Postconditioning protocol was induced by six cycles of 10s ischemia and 10s reperfusion at the onset of the reperfusion. CsA (0.5 µM or 5 µM) was administered 15 minutes before ischemia. Myocardial infarct size was estimated by triphenyltetrazolium chloride (TTC) staining. Cardiomyocyte apoptosis was assessed by TUNEL staining and creatine kinase-MB (CK-MB) was analyzed from coronary effluent., Results: In normocholesterolemia (NC) groups, infarct size, cardiomyocyte apoptosis rate and release of CK-MB were significantly reduced after IPO. These reductions were completely abolished by HC, as evidenced by a similar infarct size, cardiomyocyte apoptosis rate and release of CK-MB observed between IPO-HC group and control-NC group, but were restored by IPO combinated with CsA treatment. However, CsA treatment alone could not restore cardioprotection in a state of HC., Conclusions: Ischemic postconditioning, blocked by hypercholesterolemia may due to the excessive opening of the mPTP. Inhibiting of the mPTP with CsA is able to reverse this loss of cardioprotection.

Objective: Ischemic postconditioning (IPO) and pharmacological pretreatment may reduce myocardial necrosis and apoptosis during ischemia/reperfusion. This study aimed to determine the protective effect of fasudil pretreatment combined with IPO on myocardial ischemia/reperfusion injury in rats and explore the possible mechanisms., Materials and Methods: The SD rats were induced by intraperitoneal injection of fasudil hydrochloride (1 or 10 mg/kg) 60 min before the initiation of ischemia, while the control rats were given the same volume of saline. The hearts were hung on the Langendorff perfusion apparatus and underwent 30 min global ischemia and 120 min reperfusion. The IPO protocol was induced by six cycles of 10 sec ischemia and 10 sec reperfusion at the onset of reperfusion. The hemodynamic changes were measured, myocardial infarct size was determined by triphenyltetrazolium chloride (TTC) staining, cardiomyocyte apoptosis was detected by TUNEL staining, lactate dehydrogenase (LDH) was analyzed from coronary effluents, phosphorylation of Akt and eNOS, as well as expression of Bcl-2 and Bax were measured by western blotting analysis., Results: The high-dose fasudil (10 mg/kg) pretreatment group and IPO group significantly improved post-ischemia cardiac function, reduced myocardial infarct size, attenuated cardiomyocyte apoptosis, decreased the release of LDH, increased expression of phospho-Akt, phospho-eNOS and Bcl-2, and reduced expression of Bax compared with the control group (p < 0.05). In addition, the high-dose fasudil pretreatment combined with IPO group could further improved post-ischemia cardiac function, reduced myocardial infarct size, attenuated cardiomyocyte apoptosis, decreased the release of LDH, increased expression of phospho-Akt, phospho-eNOS and Bcl-2, and reduced expression of Bax compared with the single treatment groups (p < 0.05)., Conclusions: The combination of high-dose fasudil pretreatment and IPO had a synergistic protective effect on myocardial ischemia/reperfusion injury, which was mediated via upregulating the PI3K/Akt/eNOS pathway, increasing expression of antiapoptotic Bcl-2, and decreasing expression of proapoptotic Bax.