Background. We conducted a systematic review and meta-analysis of existing literature to evaluate the different outcomes of microRNAs (miRNAs) in diabetic nephropathy (DN), including urinary albumin excretion rates, urinary albumin creatinine rates, glomerular filtration rate, HbAc1, and creatinine.Methods. Electronic databases including PUBMED, MEDLINE, and EMBASE were searched for eligible publications to July 2018. The following comparisons between treatment groups were included: normal group versus DN group; control group versus micro/macroalbuminuria group.Results. Twelve eligible studies that included 2500 participants were finally recruited in this meta-analysis. Fifteen miRNAs (miRNA-21, miRNA-181b, miRNA-194, miRNA-30, miRNA-215, and others) were upregulated whereas seven miRNAs (miRNA-26a, miRNA-126, miRNA-424, miRNA-574-3p, miR-223, miR-155, and miR-192) were downregulated in the DN group compared with control groups. The miR-133b, miR-342, miR-30, miR-192, miR-194, and miR-215 were significantly correlated in urinary albumin excretion rates (r=0.33, 95% CI= 0.26-0.39). miR-192, miR-217, miR-15b, miR-34a, and miR-636 were correlated with urinary albumin creatinine rates (r=0.69; 95% CI=0.12-0.92), while miR-133b, miR-345, miR-33, miR-326, miR-574-3p, miR-126, miR-217, miR-15b, miR-34a, and miR-636 were significantly correlated with HbAc1 (r =0.23, 95% CI = 0.15-0.31). There were twelve miRNAs that were closely related to the glomerular filtration rate (r=0.28, 95% CI =0.21-0.34). Creatinine (r=0.33, 95% CI = 0.22-0.40) was significantly different between normal and DN groups.Conclusions. The meta-analysis acquired the correlations between miRNAs and outcomes including UAER, UACR, eGFR, HbAc1, and creatinine in DN. It suggested that miRNAs may participate in the pathogenesis of DN process.

Purpose. The current study aims to examine the effects of advanced glycation end products (AGEs) on the microRNA (miRNA) expression profile in the kidney tissues of rats. Methods. Wistar rats were randomly divided into three equal experiment groups: the AGE group, the RSA group, and the control group. The rats in the AGE group and the RSA group were administered with advanced glycation end products (AGEs) and rat serum albumin (RSA) via the tail vein, respectively, whereas the control group received PBS. Total RNA was prepared from the rat kidney tissues, and the miRNA expression profiles in different experiment groups were compared by microarray analysis. The expression levels of selected differential miRNAs were verified by RT‐qPCR. Target gene prediction was conducted using algorithms such as TargetScan, miRanda, and PICTar. Functional analysis was performed to determine the putative biological roles of the validated miRNAs. Results. The microarray study revealed 451 upregulated and 320 downregulated miRNAs in the AGE group compared with the RSA group (p < 0.05). Seven miRNAs, including miR‐21‐5p, miR‐92b‐3p, miR‐140‐3p, miR‐196a‐5p, miR‐181b‐5p, miR‐186‐5p, and miR‐192‐5p, were screened and verified using RT‐qPCR, of which, the change of miR‐92b‐3p was the most obvious according to the miRNA expression different multiple and p value. Furthermore, the expression trend of miR‐92b‐3p measured by RT‐qPCR was shown to be consistent with the microarray results. Bioinformatics analysis and luciferase reporter assay identified Smad7 was a direct target of miR‐92b‐3p. Both immunohistochemical and western blotting showed that Smad7 expression was significantly suppressed in the kidney tissues from the AGE group compared with the control and RSA groups. Conclusion. The results of the current study suggested that miR‐92b‐3p could mediate AGE‐induced development of renal abnormalities through targeting Smad7 in rats with DN.

Diabetic nephropathy (DN) is a major cause of end‐stage renal disease throughout the world; until now there is no specific drug available. In this work, we use herba artemisiae capillaris extract (HACE) to alleviate renal fibrosis characterized by the excessive accumulation of extracellular matrix (ECM) in rats, aiming to investigate the protective effect of the HACE on DN. We found that the intragastric treatment of high‐dose HACE could reverse the effect of streptozotocin not only to decrease the level of blood glucose and blood lipid in different degree but also further to improve renal functions. It is worth mentioning that the effect of HACE treatment was comparable to the positive drug benazepril. Moreover, we found that HACE treatment could on one hand inhibit oxidative stress in DN rats through regulating enzymatic activity for scavenging reactive oxygen species and on the other hand increase the ECM degradation through regulating the activity of metalloproteinase‐2 (MMP‐2) and the expression of tissue transglutaminase (tTG), which explained why HACE treatment inhibited ECM accumulation. On the basis of above experimental results, we conclude that HACE prevents DN development in a streptozotocin‐induced DN rat model, and HACE is a promising candidate to cure DN in clinic.

Norfloxacin (NORF) is a broad-spectrum quinolone that is widely utilized for the treatment of various bacterial infections and is considered one of the most commonly used fluoroquinolone antibiotics. However, NORF’s clinical utility is limited by its poor water solubility and relatively low oral bioavailability. This study presents an optimization and synergistic enhancement approach through salt/co-crystal, aiming to maximize the biopharmaceutical properties of NORF with the use of phenolic acid. Following this strategy, two new hydrate salts of NORF with phenolic acid, namely, NORF—3,5-DBA hydrate (salt 1) and NORF—VA hydrate (salt 2), were prepared and systematically confirmed. Two hydrate salts were produced by means of the slow evaporation crystallization method, and the structures were determined through single-crystal X-ray diffraction (SCXRD). Additionally, powder X-ray diffraction (PXRD), Fourier-transform infrared (FT-IR) spectroscopy, differential scanning calorimetry (DSC), thermogravimetric analysis (TGA), and high-performance liquid chromatography (HPLC) were applied to analyze the features of the two salts. The experimental results indicated that the formation of the two salts could enhance the solubility and improve the release behavior of NORF. Interestingly, the physicochemical properties of NORF were significantly improved as a result, leading to an enhancement in its antibacterial activity. This was demonstrated by the enhanced inhibition of bacterial strains and the lower minimum inhibitory concentration values.

Diabetic cardiomyopathy (DCM), one of the most severe complications of diabetes, is closely associated with oxidative stress (OS) in its development and progression. Studies have shown that plant antioxidants play an important role in the prevention and treatment of DCM by modulating redox signaling and regulating the sources of reactive oxygen species (ROS) generation. However, most existing evidence comes from animal and cellular experiments, and clinical data are limited. In addition, their clinical application faces challenges, including poor bioavailability and difficulty in standardizing active ingredients. Therefore, this review focuses on the role of plant antioxidants in regulating myocardial oxidative stress and maintaining redox homeostasis, and explores their potential clinical applications and current limitations. This review aims to provide a theoretical basis and guidance for the prevention and treatment of DCM using plant antioxidants.

Background: Genistein, an isoflavone abundant in soybeans and other legumes, has shown antiviral activity against several viruses. Its effects on enteroviruses, particularly EV71—the causative agent of hand, foot, and mouth disease (HFMD)—remain incompletely understood. Methods: In vitro assays were used to evaluate replication inhibition of EV71, assess mechanistic effects, and determine the compound’s broad-spectrum activity against other enteroviruses (EV68 and CA6). In vivo experiments in neonatal mice were conducted to further elucidate the role of genistein in EV71 replication. Results: Genistein inhibited EV71 replication, as evidenced by reduced viral genome copies, decreased viral protein expression, and lower virion numbers. The compound also reduced replication of EV68 and CA6. Mechanistically, autophagy inhibition contributed to the suppression of EV71 replication, and restoring autophagy attenuated this effect. Additionally, genistein caused a G2/M cell cycle arrest, contributing to impaired EV71 replication. In neonatal mice, genistein conferred protection against EV71-associated disease. Conclusion: The compound effectively suppresses EV71 replication and mitigates EV71-induced pathology, with concurrent activity against EV68 and CA6, and involves autophagy modulation and cell cycle disruption as part of its antiviral mechanism.