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To investigate the effect of oleanolic acid (OA) on the differentiation of neural stem cells (NSCs) induced by A[Formula: see text] via regulating the JAK/STAT signaling pathway, a neurotoxicity cell model involving the induction of NSCs by soluble A[Formula: see text] (5 [Formula: see text]M) was used. The WST-1 method and immunofluorescence tests were used respectively to detect the activity of cell model and the expression of GFAP[Formula: see text]/DAPI and Tubulin[Formula: see text]/DAPI. Western blotting and real-time PCR analyses were used to observe the effects of OA on NSCs differentiation by examining key targets of the JAK/STAT signal transduction pathway. Compared with normal NSCs, A[Formula: see text]-induced NSCs had down-regulated expression of Ngn1 and up-regulated STAT3 expression and phosphorylation, and inhibited neuronal differentiation. OA treatment effectively inhibited the A[Formula: see text]-induced activation of JAK/STAT signaling, with a significant increase in Ngn1 expression and a significant decrease in p-STAT3/STAT3. These results indicate that OA could inhibit the excessive differentiation of NSCs into astrocytes by down-regulating JAK/STAT signaling which might retard the progress of AD.

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The present study aimed to explore the correlation between the dynamic serum levels of phospholipase A2 receptor (PLA2R), aldose reductase (AR) and superoxide dismutase 2(SOD2) antibodies with disease activity and treatment response in patients with idiopathic membranous nephropathy (IMN). The present study included 56 patients with IMN who were diagnosed through a renal biopsy and presenting with nephrotic syndrome. The patients were divided into two treatment groups: One treated with cyclophosphamide (CTX) and one with tacrolimus (FK506). Serum was collected prior to treatment, and at 1, 3, 6, 9 and 12 months after the start of the 12-month-long therapy. Samples were tested by ELISA to measure anti-PLA2R, anti-AR and anti-SOD2 antibody titers. In addition, urinary protein excretion, serum albumin (Alb) and other blood biochemical indexes were measured. Theanti-PLA2R antibody positivity rate was 71.43% in the patients prior to treatment. After 12 months of treatment, proteinuria and PLA2R antibody levels were decreased, whereas serum Alb was increased. There was no significant difference of remission rates between the CTX and FK506 groups. In conclusion, the results of the present study indicate that the anti-PLA2R antibody level is correlated with the severity of IMN, whereas anti-AR and anti-SOD2 antibody levels are not. In addition, there was no significant difference between the CTX and FK506 groups in regards to the remission rates of patients with IMN.