ABSTRACT
To explore the protective effectof Likun preparation No.1 on bone marrow suppression injury in mice and the possible mechanism. Methods Sixty male BALB/c mice were randomly divided into normal control group, 5-Fu model group, positive control group(rhG-CSF) and Likun preparation No.1 groups with low, medium and high doses. Myocardial inhibition was established by intraperitoneal injection of 5-fluorouracil once. After seven days of administration, blood routine analysis was performed. Serum levels of TNF-α and IL-2 were detected by ELISA. The expression of p-JAK2 and p-STAT5 protein in spleen tissues were determined by Western blot. Results After given the Likun preparation No.1, the symptoms of diarrhea in mice were alleviated, body weight increased(P < 0.05), and white blood cells, platelets and lymphocytes also increased(P < 0.05). ELISA test showed that the serum level of IL-2 in Likun preparation high-dose group was higher than that in model group(P < 0.05), and the TNF-α content was lower than that in model group(P < 0.05). Western blot analysis showed that compared with model group, the expression of p-JAK2 and p-STAT5 protein in spleen of mice in Likun preparation group was up-regulated(P < 0.05). Conclusions The Likun preparation No.1 has protective effect on 5-Fu-induced myelosuppression in mice. The molecular mechanism may be related to the up-regulation of p-JAK2 and p-STAT5 protein expression, the promotion of IL-2 production and the reduction of TNF-α secretion.
ABSTRACT
Objective To investigate the protective effect of trichostatin-A (TSA) on cerebral ischemia/reperfusion injury via Janus kinase/signal transducer and activator of transcription (JAK/STAT) signal pathway.Methods 36 male SD rats were randomly (random number) divided into 3 groups:shamoperated group,ischemia/reperfusion (I/R) group and TSA group.Rat model of middle cerebral artery occlusion/reperfusion (MCAO) was established using a modified filament method.No occlusion was applicated to the sham-operated group.TSA group was injected with TSA 0.05 mg/kg via penile vein,20 minutes before operation.Reperfusion was carried out 24 hours after modeling.Longa 5 score was used to assess the neurological function,and TTC staining was applied to calculate the percentage of cerebral infarction area,The expression of JAK2 and p-JAK2 proteins was detected by Elisa.Results The low expression of JAK2 was observed in each group,and there was no statistical difference between groups (P =0.266).Compared with I/R group,TSA group had lower score in cerebral ischemia-reperfusion injury assessment (P=0.019),smaller area of cerebral infarction (P ＜0.01),reduced expression of p-JAK2 (P =0.009),all of which were of significant difference.Condusions TSA can reduce the cerebral ischemia/reperfusion injury via JAK/STAT signal pathway by down regulating p-JAK2 expression.
ABSTRACT
Objective To investigate the effects of rapamycin on p-JAK2,STAT3,p-STAT3 and PCNA in ranal tissue of IgAN rats.Methods The animal models of IgA nephropathy were devided into control group,IgAN model group,losartan group and rapamycin group.The clinical efficacy of rapamycin,and its influences on the protein and mRNA expressions of STAT3,p-STAT3,p-JAK2 and PCNA were determined by western blot,RT-PCR and immunohistochemical techniques respectively.Results The protein and mRNA expressions of p-STAT3,STAT3,p-JAK2 and PCNA were significantly increased in kidney of IgAN rats(P