Abstract. Nephrotic syndrome (NS) is the most common kidney disease in clinical practice and may lead to end-stage renal failure. Astragalosides (AST) have been clinically tested for the treatment of NS, but their mechanism of action has remained to be elucidated. The aim of the present study was to investigate the effect of AST on the structure and function of podocytes with adriamycin (ADR)-induced damage and to elucidate the underlying molecular mechanisms. The mouse podocyte clone 5 (MPC5) immortalized mouse podocyte cell line was treated with 0.5 µmol/l ADR to establish a podocyte injury model. The MPC5 podocytes were divided into a control group, a podocyte injury group and a low-, medium-and high-concentration AST treatment group. The results indicated that the survival rate of the podocyte injury group was significantly decreased compared with that in the control group and each AST-treated group had an increased survival rate compared with that in the podocyte injury group. Furthermore, each dose of AST significantly inhibited the ADR-associated increases the levels of lactate dehydrogenase and malondialdehyde and the decrease in the activity of superoxide dismutase in MPC5 podocytes. In addition, AST improved the migration ability of MPC5 podocytes and suppressed the cytoskeletal rearrangement associated with ADR-induced damage. Furthermore, matrix metalloproteinase (MMP)-2 and -9 were decreased in the podocyte injury group, which was inhibited by different concentrations of AST. Thus, AST was able to maintain the balance of oxidative stress in podocytes cultured with ADR and protect them from ADR-induced injury. The mechanism may be associated with the upregulation of MMPs.
Genotype C was the most frequent genotype in the described group of patients with HBV-GN, and the liver and kidney damage indicators were more likely to occur in patients with genotype C.
Subsequently to the publication of this article, the authors have realized that name of the second author (who is the joint first author on the study) was spelt incorrectly. This appeared as "Yuan-Chun Sun", whereas the name should have been published as "Yuan-Chun Song". The corrected name is featured below.
Cerebral palsy (CP) is a neurodevelopmental and motor disorder syndrome threatening children’s physical and mental health. Hypoxic-ischemic brain injury and inflammation have been considered as the main causes of CP. Mesenchymal stem cells (MSCs) can repair brain tissue damage, and many studies have proved that exosomes from MSCs have a critical advantage in the central nervous system (CNS) disease. Therefore, this study aimed to explore the improvement effect of human umbilical cord MSC (hUC-MSC)-derived exosomes on CP and whether synergistic action existed when combined with mouse nerve growth factor (mNGF). Therefore, the exosomes were isolated from hUC-MSCs and examined using electron microscopy, particle size, and Western blot (WB). A CP model was constructed by hypoxic induction after unilateral common carotid artery ligation combined with lipopolysaccharide (LPS) infection. The pathological damage of neuron tissue and synaptic structure in the hippocampus was determined using a light microscope after hematoxylin-eosin (HE) staining and transmission electron microscopy, respectively. The survival of neurons was analyzed using Nissl staining. The WB analysis was performed to monitor postsynaptic density 95(PSD-95) and synaptophysin(SYN) protein levels. The results showed that exosomes released by hUC-MSCs could ameliorate the motor function in mice with CP by rescuing the impaired brain tissue, synaptic structure, and neuronal function with increased PSD-95 and SYN levels. When the exosome was combined with mNGF, an improvement in CP was found. The results indicated that the intravenously injected hUC-MSC-exosomes and intraperitoneal administration of mNGF alleviated the nerve function injury in mice with CP.
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