Objective To explore the protective effect and mechanism of astaxanthin (AST) on the acute kidney injury induced by iohexol in rats.Method Thirty rats were randomly divided into five groups:control group (Ctrl);iohexol group (CM);astaxanthin group (AST,100 mg/kg),low astaxanthin dose group (LAST+CM,50 mg/kg) and high astaxanthin dose group (HAST+CM,100 mg/kg),6 in each group.The rats in AST,LAST+CM,HAST+CM groups were administrated with AST by oral gavages using an intubation needle for 10 consecutive days.The rats in Ctrl and CM groups rats in Ctrl,CM groups were given with dissolvant instead in equal volume.Except for the Ctrl and AST groups,on day 8,rats were given indomethacin,L-NAME and iohexol in their femoral vein under chloral hydrate anesthesia to build a contrast induced-nephropathy (CIN) model.At the end of the experiment (72 h after CIN induction),all rats were sacrificed.The Scr level,BUN level,renal histology,renal tissue activities in superoxide dismutase (SOD),catalase (CAT),glutathione peroxidase (GPx),Glutathione (GSH) and level of malondialdehyde (MDA) were performed.Apoptosis of renal cells was detected by Bcl-2,Bax and Caspase-3 p17 with Western blot.Results Compared with Ctrl group,the levels of Scr,BUN were significantly increased in CM group (all P ＜ 0.01);while compared with CM group,the indicators were decreased in treatment groups (P ＜ 0.01).Renal tubular structure damage,medulla congestion,loss of brush border,vacuolar degeneration,apoptosis and proteinaceous casts were observed in the CM group,and the renal injury scores were higher compared with Ctrl group (P ＜ 0.05),however,administrated with AST could significantly improve the changes (P ＜ 0.05).Oxidative stress indicators showed that MDA level were increased while SOD,GPx,GSH activities were significantly decreased at CM group (all P ＜ 0.05),and the indicators above were ameliorated in treatment groups (all P ＜ 0.05).Western blot showed that the expression of Bcl-2 was down-regulated while the Bax,Caspase 3 p17 was up-regulated respectively at CM group (P ＜ 0.05),while the HAST+CM group could prevent the changes.Conclusions Iohexol can results in oxidative stress increased in kidney,which activate Caspase-3 p17 signal path,down-regulated Bcl-2 expression,up-regulated Bax expression respectively,and lead to cell apoptosis.AST can ameliorate the changes,especially with high AST dose,which suggest that the possible protection mechanism is by ameliorating oxidative stress and inhibiting apoptosis pathways.

AIM:There is little evidence proving the molecular mechanism of WenxinKeli ( WXKL) .This study tried to explore the gene ex-pression profile and pathology alteration of WXKL-treated rabbits with myocardial infarction .METHOD: Twenty male adult rabbits were randomly divided into 4 groups:sham, model, WXKL and captopril groups .Model, WXKL and captopril groups underwent the ligation of the left anterior descending coronary artery , while sham group went through an identical procedure without ligation .WXKL (817 mg? kg-1? d-1), captopril (8 mg? kg -1? d-1) and distilled water (model and sham) were administered orally to the rabbits. 4 weeks later, hearts were taken out for expression chip and pathological staining (HE, Masson and TUNEL) after echocardiography. RESULT:WXKL could down-regulate genes associated with inflammation (CX3CR1, MRC1, and FPR1), apoptosis (cathepsin C and TTC5) and neuro-hormonal system (ACE and EDN1), and up-regulate angiogenesis promoting gene like RSPO 3, which explained why WXKL group represented with better cardiac function , less histopathological injury and slighter apoptosis .CONCLUSION:WXKL plays an important role in suppressing inflammation , inhibiting renin-angiotensin system and alleviating apoptosis , and might be a promising Chinese medicine in treating patients with myocardial infarction .

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.

BACKGROUND:Buprenorphine transdermal patches have the characteristics of stable blood concentration, long duration of analgesia, respiratory depression and less side effects, which have been widely used in the treatment of moderate to severe chronic pain. OBJECTIVE:To observe the clinical outcome of preoperative analgesia by buprenorphine transdermal patches for pain management after posterior lumbar surgery. METHODS: Eighty patients scheduled for posterior lumbar decompression and interbody fusion under general anesthesia were enroled, 45 males and 35 females, aged 42-71 years, who were randomly divided into two groups, 40 cases in each group: experimental group and control group. In the experimental group, buprenorphine transdermal patches were given 2 days prior to the internal fixation, and intravenous injection of parecoxib was given for postoperative pain management. In the control group, placebo patches were given prior to the internal fixation, and self-control vein analgesia pump and intravenous injection of parecoxib were given for postoperative pain management. Visual analog scale scores were recorded at 6, 12, 24, 48 hours after surgery as wel as doses of tramadol hydrochloride and pethidine hydrochloride used postoperatively and side effects. The patient's satisfaction, drainage and blood count, erythrocyte sedimentation rate, C-reactive protein level at 48 hours postoperatively were detected and recorded in the two groups. RESULTS AND CONCLUSION:There was no significant difference between these two groups in visual analog scale scores, dosage of tramadol hydrochloride and pethidine hydrochloride used postoperatively, postoperative drainage amount, leukocyte count, erythrocyte sedimentation rate and C-reactive protein level (P > 0.05). Postoperative incidence of nausea, vomiting and delirium was lower in the experimental group than the control group (P < 0.05), but the patient's satisfaction in the experimental group was better than that in the control group (P< 0.05). These findings indicate that buprenorphine transdermal patches have better preemptive analgesia for posterior lumbar surgery, with less adverse effects and better patient's satisfaction.

Objective To investigate the molecular mechanisms of synergistic effects of BFA and CDDP on human lung cancer GLC-82 cells, and to test the levels of PERK-ATF4 pathway. Methods GLC-82 cells were incubated with 50 ng/mL of BFA or/and 2 μg/mL of CDDP for 24 or 48 hours. The levels of PERK, p-PERK and ATF4 in GLC-82 were analyzed by real-time PCRand/or Western Blot. Results The levels of PERK were lowest in CDDP group, but higher in BFA group (P < 0.05), the highest in group of BFA+CDDP (P < 0.05 or P < 0.01). The p-PERK level decreased in group of BFA+CDDP (P < 0.05 or P < 0.01). There was no significant change of ATF4 expression in CDDP group, but ATF4 expression increased slightly in BFA group, and increased further in group of BFA+CDDP (P < 0.05 or P < 0.01)which was also higher than that in BFA group or CDDP group (P < 0.05 or P < 0.01). Conclusions The upregulated levels of PERK and ATF4 by the combination of BFA and CDDP may be one of the mechanisms of synergistic anti-cancer effect of BFA and CDDP on GLC-82 cells.

Objective To systematically evaluate the effectiveness and safety of interleukin-2 plus cisplatin for treating ma-lignant pleural effusion(MPE)to provide a basis for clinical treatment strategy.Methods CBM,CNKI,VIP,Wanfang,Pubmed, Embase,Cochrane library clinical trial registration database were systematically retrieved.The randomized controlled trial(RCT) quality assessment criteria of Cochrane collaboration network was adopted for including the study quality.The data were extracted by meta analysis.Results (1)Thirty-four RCT involving 2 037 MPE patients were included,the quality of included RCT was ordi-nary;(2)compared with simple cisplatin,the merged RR values and their 95%CI of meta-analysis for ORR,fever,were 1.45 (1.36-1.54),2.37 (1.53 -3.66),respectively,the differences between the two groups were statistically significant(P <0.05 ). The merged RR values and their 95%CI of meta-analysis for leukopenia,myelosuppression and thoracalgia were 0.81 (0.61 -1.07),0.83(0.62-1.11)and 1.04(0.84-1.29)respectively,the differences between two groups were not statistically significant (P >0.05).Conclusion This study indicates that IL-2 plus cisplatin can significantly improve the clinical curative effect in the pa-tients with MPE,but has the adverse reactions of fever,etc.and the quality of included RCT is general.

Objective To investigate the synergistic effects of tannic acid(TA) and cis-dichlorodiamine platinum(CDDP) on hepatocellular carcinoma HepG2 cells and its activation situation of endoplasmic reticulum stress(ERS) pathway.Methods Human hepatocellular carcinoma HepG2 cells were divided into the control group,TA group,CDDP group and TA+CDDP group,and were cultured in vitro for 24 h.The growth inhibitory effect of medication on HepG2 cells was detected by MTT assay.The pharmacodynamics synergistic effect between the two drugs was analyzed by the drug interaction index,drug dose reduction index and equivalent graphical method.The nucleus changes were observed by DAPI staining.Real time fluorescent quantitative PCR(q-RT-PCR) and Western blot were used to detect the levels of ERS markers glucose regulated protein (GRP)78 and GRP94.Results TA and CDDP had dose-dependent growth inhibition effect on HepG2 cells,their median effective concentrations(IC50) were 360.00 μmol/L and 1.80 μg/mL respectively.The combination treatment of 180.00 μmol/L TA and 0.90 μg/mL CDDP on HepG2 cells could enhance the inhibitory effect on cell growth.Ta and CDDP had synergistic effect for inhibiting hepatocellular carcinoma cells growth.Compared with the TA group and CDDP group,cell shrinkage and rounding were accelerated in the combined group,apoptotic cells were increased,nuclear had pyknosis,irregular edge and dense staining,nuclear fragmentations were increased and the expressions of GRP78 and GRP94 were up-regulated.Conclusion TA can enhance the effect of CDDP on anti-hepatic carcinoma HepG2 cells,and the synergy mechanism may be related to the activation of ERS pathway.

Guanosine triphosphate cyclohydrolase 1 (GTPCH1) is a protein encoded by the GCH1 gene,which catalyze GTP to tetrahydrofolinine (BH4) under physiological condition.BH4 is a coenzyme of aromatic amino acid hydroxylase and a cofactor of nitric oxide synthases.BH4 involves in the synthesis of various hormones and neurotransmitters and plays an important role in a series of pathophysiological processes in vivo.Recent studies showed that GTPCH1 is involved in the pathogenesis of neuropathic pain,doparesponsive dystonia,cancer and cardiovascular diseases.In this review,we will discuss the role of GTPCH1 in those diseases mentioned above.

Objective:To explore the association of -592A/C and -1082A/G single nucleotide polymorphism in interleukin (IL)-10 gene with susceptibility to serofast in patients with syphilis.Methods:The SNPs of -592A/C and -1082A/g in the promoter region of IL-10 were detected by multiple single base extension (SNaP-shot) assay in 123 patients with syphilis(syphilis group), 118 patients with seronegative syphilis (seronegative syphilis group) and 120 healthy controls (healthy control group). The clinical characteristics, genotypes and allele frequencies of different subjects were compared.Results:There was no significant difference in age and gender between syphilis group, seronegative syphilis group and healthy control group ( P>0.05). There was no significant difference in the number of sexual partners, initial rapid plasma reagin test for syphilis (RPR) titer, stage, and Jihai reaction between the syphilis group and seronegative syphilis group ( P>0.05). There was no significant difference in the genotype and allele frequency of -592A/C and -1082A/G in the promoter region of IL-10 between the syphilis group, seronegative syphilis group and the control group ( P>0.05). Conclusions:There seems to be no evidence for association between -592A/C and -1082A/G single nucleotide polymorphism in IL-10 gene and susceptibility to serofast in patients with syphilis.

Objective To report 9 HIV-negative patients with talaromycosis marueffei (TSM)complicated by Sweet syndrome,and to analyze the relationship of the anti-interferon-γ (anti-IFN-γ)autoantibody with TSM complicated by Sweet syndrome.Methods HIV-negative patients with TSM complicated by Sweet syndrome were collected from the First Affiliated Hospital of Guangxi Medical University between 2013 and 2018.Their clinical and laboratory data were analyzed retrospectively.Meanwhile,19 HIV-positive patients with TSM and 107 health checkup examinees served as controls.Anti-IFN-γ autoantibody was detected in peripheral blood samples of the patients and controls.Results A total of 9 HIV-negative patients with TSM (5 males and 4 females) were included in this study,and the age of onset ranged from 38 to 60 years.The 9 patients all presented with disseminated infections,manifesting as long-term irregular fever,multiple lymph node enlargement,cough,emaciation and anemia.All of the 9 patients met the diagnostic criteria for classical Sweet syndrome,and microbiological examination of Sweet syndrome lesions was negative.Besides Talaromyces marneffei,6 patients also were infected with nontuberculous mycobacteria,4 with varicella-zoster virus,and 2 with Salmonella.All the 9 HIV-negative patients with TSM were positive for anti-IFN-γ autoantibody,while the 107 healthy controls and 19 HIV-positive patients with TSM were negative for anti-IFN-γ autoantibody.Conclusion Anti-IFN-γ autoantibody may be associated with HIV-negative TSM complicated by Sweet syndrome.