Objective To explore the relationship between the changes of lactate dehydrogenase (LDH) and cholinesterase (CHE) activities and death from hanging of bound upper limbs (DHBL). Methods After the animal model of DHBL was established, the LDH and CHE activities in the serum and tissues including diaphragm muscle and musculi gastrocnemius were determined. Results In DHBL group, LDH activity decreased significantly in diaphragm muscle as compared with that in musculi gastrocnemius (P0.05). In comparison with the control group, LDH activity lowered greatly in the diaphragm muscle(P0.05). Significant decrease in serum LDH in the DHBL group as compared with control group (P0.05). Conclusion Decrease in the LDH activity may be associated with hanging posture of bound upper limbs.

Objective:To study the protective effect of polysaccharide from Rose roxburghii Tratt (RRTP-1) on neural stem cells damaged by glutamic acid (Glu). Method: RRTP-1 was obtained by ion exchange column chromatography and gel chromatography. The neural stem cells were cultured from the striata of fetal mice and damaged by glutamic acid to simulate hypoxic-ischemic brain injury. The cultures were divided into control group, glutamic acid group and test groups in which different doses of RRTP-1 were added with glutamic acid. The death rate of neural stem cells damaged by Glu and LDH leakage were observed. Results:The neural stem cells damage of test groups were alleviated,and the death rate of neural stem cells and LDH leakage of high dose test group were significantly lower than glutamic acid group. Conclusion:RRTP-1 has remarkable protective effect on neural stem cells damage.

Increased microglial activation and neuroinflammation within autonomic brain regions such as the rostral ventrolateral medulla (RVLM) have been implicated in stress-induced hypertension (SIH). Prorenin, a member of the brain renin-angiotensin system (RAS), can directly activate microglia. The present study aimed to investigate the effects of prorenin on microglial activation in the RVLM of SIH rats. Rats were subjected to intermittent electric foot-shocks plus noise, this stress was administered for 2 h twice daily for 15 consecutive days, and mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were monitored. The results showed that MAP and RSNA were augmented, and this paralleled increased pro-inflammatory phenotype (M1) switching. Prorenin and its receptor (PRR) expression and the NLR family pyrin domain containing 3 (NLRP3) activation were increased in RVLM of SIH rats. In addition, PLX5622 (a microglial depletion agent), MCC950 (a NLRP3 inhibitor), and/or PRO20 (a (Pro)renin receptor antagonist) had antihypertensive effects in the rats. The NLRP3 expression in the RVLM was decreased in SIH rats treated with PLX5622. Mito-tracker staining showed translocation of NLRP3 from mitochondria to the cytoplasm in prorenin-stimulated microglia. Prorenin increased the ROS-triggering M1 phenotype-switching and NLRP3 activation, while MCC950 decreased the M1 polarization. In conclusion, upregulated prorenin in the RVLM may be involved in the pathogenesis of SIH, mediated by activation of the microglia-derived NLRP3 inflammasome. The link between prorenin and NLRP3 in microglia provides insights for the treatment of stress-related hypertension.