Objective To investigate the antimicrobial and antitumor activities of extracts from the root of mangrove plant,Kandelia candel.Methods Micro-dilution and MTT method were used to test the antimicrobial and antitumor activities of extracts from the root of K.candel.Results The petroleum ether extracts of root could inhibit the growth of Staphylococcus aureus,S.epidermidis,Bacillus subtilis and Sarcina lutea with the minimal inhibitory concentration(MIC) of 3.125 mg?mL-1,1.5625 mg?mL-1,0.78125 mg?mL-1 and 3.125 mg?mL-1 respectively.The ethyl acetate extracts and ethyl alcohol extracts could inhibit the growth of S.epidermidis with MIC of 3.13 mg?mL-1 and 6.25 mg?mL-1 respectively.At the same time,the petroleum ether extracts could inhibit the proliferation of tumor cells,such as SMMC-7721,B16,BGC803 and HepG2 with IC50 of 355.2?g?mL-1,378.6?g?mL-1,275.6?g?mL-1 and 411.6?g?mL-1 respectively,while the other extracts could stimulate the proliferation of tumor cells apparently.Conclusion The antimicrobial and antitumor activities of extracts from the root of K.candel indicate the potential pharmaceutical usage of this plant.

Objective:To observe the change of periphery and centra lymphocyte subsets at the crest-time of MOG_(35-55) induced EAE disease in mice,and to explore the alteration of cellular immunity and humoral immunity in the invasion process in EAE.Methods:MOG_(35-55) was used to establish EAE model in femina C57BL/6 mice.The behavioral changes and the histological scores were recorded after the mice were immuned .The changes of CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ on periphery and centra lymphocytes in spleen,brain and spinal cord were analyzed by flow cytometry.Results:The CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ lymphocytes were detected in the brain and spinal cord of EAE group mice,but they were not detected in CFA control group.The CD3~+CD4~+ and CD3+CD8+lymphocytes in the spleen of EAE crest-time group were lower than those in CFA control group(P＜0.05).The B220~+ lymphocytes were obviously higher than in the CFA control group (P＜0.01).And CD4~+CD25~+ lymphocytes were slight higher than the CFA control group.Conclusion:At the crest-time during EAE,the CD3~+CD4~+,CD3~+CD8~+lymphocytes of spleen reduced obviously,B220~+ lymphocytes increased markedly,and the CD4~+CD25~+ lymphocytes just have the increasing trend.It indicates that cellular immunity and humoral immunity coregulated the patho-process at the crest-time of EAE,T lymphocytes and B lymphocytes all played important roles in the pathogenesy of EAE.

Objective:Methamphetamine(METH)is an illicit psychoactive substance that can damage various organs,with the urinary system being one of its significant targets.This study aims to explore the role of microtubule affinity-regulating kinase 4(MARK4)in METH-induced acute kidney injury(AKI). Methods:A total of 10 healthy adult male C57BL/6 mice were randomly divided into a control group and a METH group,5 mice in each group.The METH group was administered METH(20 mg/kg,intraperitoneally,once daily for 3 consecutive days),while the control group received an equal volume of physiological saline.The mice were executed 24 hours after the final injection,and the success of the AKI model was detected by blood serum creatinine,blood urea nitrogen,and renal HE staining.Proteins differentially expressed between kidney tissues with METH-induced AKI and normal kidney tissues were screened by proteomics techniques and subjected to gene ontology(GO),Kyoto Encyclopedia of Genes and Genomes(KEGG)and bioinformatics analysis.The accuracy of proteomic data was validated using Western blotting,and the expression levels of MARK4 and cleaved caspase-3 in mouse kidneys were measured.We further explored the role of MARK4 in METH-induced AKI.Firstly,a METH toxicity model was established in BUMPT cells to screen the appropriate concentration and time of METH treatment;the viability of BUMPT cells after METH treatment and the expression of cleaved caspase-3 were detected by interfering with MARK4 expression through inhibitors. Results:The proteomic analysis of kidney tissues from METH and control groups screened for a total of 17 differentially expressed proteins,of which 11 were up-regulated and 6 were down-regulated(all P＜0.05).The expression levels of MARK4 and cleaved caspase-3 were elevated in the kidneys of METH-treated mice(both P＜0.05).The activity of BUMPT cells gradually decreased with increasing METH treatment concentration(all P＜0.05),where the viability of BUMPT cells decreased to about 60％after METH treatment at 4 mmol/L.Compared with the control group,expression levels of MARK4 and cleaved caspase-3 were increased with higher METH concentrations and longer exposure times in a concentration-and time-dependent manner(all P＜0.05).Inhibition of MARK4 expression improved METH-induced decrease in BUMPT cell activity,down-regulated the expression of cleaved caspase-3,and decreased the apoptosis of BUMPT cells induced by METH. Conclusion:MARK4 is highly expressed in a mouse model of METH-induced AKI,and MARK4 mediates METH-induced AKI by regulating cell apoptosis.