To explore the protective effect of Angelica sinensis polysaccharide(ASP)on leptospiro-sis induced by pathogenic Leptospira infection,the golden hamster model of leptospirosis was se-lected for the experiment.The Leptospira and Leptospira+ASP groups were intraperitoneally injected with Leptospira interrogans serovar Lai strain 56601(1 × 10 6 per hamster).After infec-tion,the Leptospira+ASP group was injected intraperitoneally with ASP(50 mg/kg)for three consecutive days,while the Leptospira group was injected intraperitoneally with normal saline for three days.The experiment employed methods such as daily observation of the clinical symptoms of golden hamsters,statistics of the survival status of each group of golden hamsters,pathological damage of liver,kidney,and lung,bacterial load in organs,and the expression of inflammatory cy-tokines(IL-1β and TNF-α).The results indicated that ASP could effectively alleviate the clinical symptoms of the infected hamsters,enhance the survival rate,ameliorate the pathological damage of the body,reduce the bacterial load in various organs,and mitigate tissue inflammation.This study demonstrated for the first time that ASP has a protective effect on leptospirosis,providing medication guidance for the clinical treatment of leptospirosis.

To explore the protective effect of Angelica sinensis polysaccharide(ASP)on leptospiro-sis induced by pathogenic Leptospira infection,the golden hamster model of leptospirosis was se-lected for the experiment.The Leptospira and Leptospira+ASP groups were intraperitoneally injected with Leptospira interrogans serovar Lai strain 56601(1 × 10 6 per hamster).After infec-tion,the Leptospira+ASP group was injected intraperitoneally with ASP(50 mg/kg)for three consecutive days,while the Leptospira group was injected intraperitoneally with normal saline for three days.The experiment employed methods such as daily observation of the clinical symptoms of golden hamsters,statistics of the survival status of each group of golden hamsters,pathological damage of liver,kidney,and lung,bacterial load in organs,and the expression of inflammatory cy-tokines(IL-1β and TNF-α).The results indicated that ASP could effectively alleviate the clinical symptoms of the infected hamsters,enhance the survival rate,ameliorate the pathological damage of the body,reduce the bacterial load in various organs,and mitigate tissue inflammation.This study demonstrated for the first time that ASP has a protective effect on leptospirosis,providing medication guidance for the clinical treatment of leptospirosis.

Objective To evaluate the effect of remifentanil on Toll-like receptor 2 (TLR2) mRNA expression during renal ischemia-reperfusion (Ⅰ/R) in rats.Methods Fifty-four male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 3 groups (n=18 each) using a random number table:sham operation group (group S),Ⅰ/R group and remifentanil group (group R).Renal Ⅰ/R injury was produced by clamping the bilateral renal arteries for 45 min followed by reperfusion in Ⅰ/R and R groups.Bilateral renal arteries were only exposed but not clamped in group S.Remifentanil 1.0 μg · kg-1 · min-1 was infused via the tail vein starting from 15 min before ischemia until 30 min of reperfusion in group R,while the equal volume of normal saline was given instead in S and Ⅰ/R groups.The animals were sacrificed at 15 min before ischemia and 6 and 24 h of reperfusion,and the renal specimens were obtained for examination of the pathological changes (with light microscope) and for determination of the contents of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) (by ELISA) and expression of TLR2 mRNA (by RT-PCR) and cell apoptosis (by double staining and flow eytometry).The apoptotic rate was calculated.Results Compared with group S,TLR2 mRNA expression was significantly up-regulated,and the contents of TNF-α and IL-6 and apoptotic rate were increased at 6 and 24 h of reperfusion in Ⅰ/R and R groups.Compared with group Ⅰ/R,TLR2 mRNA expression was significantly down-regulated,and the contents of TNF-α and IL-6 and apoptotic rate were decreased at 6 and 24 h of reperfusion in group R.The pathological changes were significantly attenuated in group R as compared with group Ⅰ/R.Conclusion The mechanism by which remifentanil reduces renal Ⅰ/R injury is related to down-regulation of TLR2 expression and decrease in TLR2 activity and inhibition of inflammatory responses in renal tissues and cell apoptosis in rats.

Objective To evaluate the role of mitochondria-mediated apoptosis in hippocampal neurons in sevoflurane anesthesia-induced cognitive dysfunction in aged rats.Methods Sixty healthy male Sprague-Dawley rats,aged 20 months,weighing 550-600 g,were randomly divided into 2 groups (n =30 each) using a random number table:control group (group C) and sevoflurane anesthesia group (group S).Animals inhaled pure oxygen and 3 ％ sevoflurane for 4 h in C and S groups,respectively.Ten rats were chosen at 1 and 6 days after anesthesia and hippocampal tissues were obtained for detection of cell apoptosis and mitochondrial membrane potential (MMP) (using flow cytometry) and expression of cytochrome c (Cyt c) in cytoplasm and activated caspase-3 in hippocampal neurons (by Western blot).The apoptotic rate was calculated.Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform,the percentage of time of staying at the original platform quadrant and MMP were decreased,the apoptotic rate was increased,and the expression of activated caspase-3 and Cyt c in cytoplasm was up-regulated in.group S.Conclusion The mechanism by which sevoflurane anesthesia induces cognitive dysfunction is related to the activation of mitochondria-mediated apoptosis in hippocampal neurons of aged rats.

Objective To evaluate the effect of preconditioning with nimodipine on postoperative cognitive dys function of aged rats.Methods Ninety healthy male Sprague-Dawley rats,aged 18 months,weighing 400-500 g,were randomly divided into 3 groups (n =30 each) using a random number table:nimodipine control group (group N),surgery group (group S),and nimodipine + surgery group (N+ S group).In N and N + S groups,nimodipine 1 mg/kg was intraperitoneally injected,while the equal volume of normal saline was given instead in S group.30 min later,group N inhaled pure oxygen for 2 h,and S and N + S groups inhaled 1.8 ％ isoflourane for 2 h when splenectomy was performed.Morris water maze test was performed on 1 day before operation and 1st,3rd and 7th days after operation.After the end of Morris water maze test at 1 day before operation and 1st and 7th days after operation,10 rats were sacrificed and brains were removed and hippocampi were isolated for determination of apoptosis in hippocampal neurons,intracellular [Ca2+] i in cytoplasm,and hippocampal Bcl-2 and Bax mRNA expression and for examination of ultrastructure of hippocampal neurons.Results Compared with the value before administration,the escape latency was significantly prolonged,the frequency of crossing the original platform was decreased,apoptotic rate and [Ca2+]i were increased,Bcl-2 mRNA expression was down-regulated,and Bax mRNA expression and Bax/Bcl-2 mRNA ratio were up-regulated at each time point after operation in S and N + S groups,and no significant changes were found in the parameters mentioned above in N group.Compared with group S,the escape latency was significantly shortened,the frequency of crossing the original platform was inecreased,apoptotic rate and [Ca2+]i were decreased,Bcl-2 mRNA expression was up-regulated,and Bax mRNA expression was down-regulated at each time point after operation in group N + S.Pathological changes were found in S and N + S groups and the damage was severer in S group than in N + S group.Conclusion Nimodepine preconditioning can prevent postoperative cognitive dysfunction of aged rats,and inhibition of calcium overloadinduced apoptosis in hippocampal neurons may be involved in the mechanism.