Animal models of rheumatoid arthritis(RA)especially adjuvant arthritis(AA)in rats and collagen induced arthritis(CIA)in mice have much character similar to human RA in pathological mechanism,clinical representation and so on. The models are more ideal in investigating RA and selecting drugs of anti inflammation and immunity. To discuss the pathological mechanism and the relation between animal models of RA and clinic will be important not only to research RA in pathology,physiology,nervous endocrine immunity and so on,but also to find out safety and effective drugs of treatment RA. The articl summarizes several animal models of RA in establishment,pathological and clinical changes,inflammatory immune regulation and so on.

Aim To investigate the possible mechanism of antitumor in human lung cancer cell lines A549 and NCI-H460 induced by lumiracoxib.Methods The expression of COX-2 was detected by Western blot and the levels of PGE2 and cAMP was determined by radioimmunoassay (RIA).Results COX-2 protein was highly expressed in A549 and NCI-H460 cells.After treatment with 15~240 ?mol?L-1 LUM for 24 hrs,LUM significantly decreased the level of COX-2 in A549 cells,but not in NCI-H460 cells.Compared with the control,the PGE2 production was reduced and the level of cAMP was increased after the treatment with 15,30,60,120,240 ?mol?L-1 of LUM,respectively.Conclusion The effect of Lumiracoxib on antitumor is in COX-2-dependent or-independent manner. The antitumor effect of LUM may be related to inhibiting the COX-2 activities by decreasing its secretion,up-regulating the level of cAMP,and down-regulating the level of PGE2.

Endoplasmic reticulum(ER) is a locus where proteins are modified,folded and calcium stored.The accumulation of unfolded protein and disorder of calcium ion can lead to ER stress.Early ER stress will induce unfolded protein response(UPR)which may be protective to cells.On the contrary,long-time strong ER stress will induce cell apoptosis,even death.ER stress has been suggested to be involved in some human neurodegenerative diseases.However,the exact contributions of ER stress in the various disease processes are yet unknown.This review mainly summarizes recently reported discoveries concerning ER stress associated with neurodegenerative diseases and highlights current knowledge in this field that may reveal novel insight into disease mechanisms and help to design better therapies for these disorders.

The effects of selenium-enriched yeast (Sey) on DTH in immunosuppressive mice have been investigated. It was found that Sey (30, 60, 90 mg?kg-l?d-1?6 d, ig) was able to antagonize lowered DTH by cyclophospha-mide (Cy); Meanwhile, the thymus and spleen weights were increased by Sey (30, or 60 mg?kg-1?d-1) in immunosuppressive mice. Sey also potentiated the lowered ConA and LPS-indu-ced proliferation of splenocytes in DTH mice at the doses of 30, 60, or 90 mg ?kg-1 and 60 or 90 mg?kg-1 respectively. These results suggested that Sey could enhance the functions of lymphocytes.

Aim To investigate the effect of α1-anti-trypsin Z variant (ATZ)overexpression on cell autoph-agy.Methods HEK 293T cells were transfected with pcDNA3.1 zeo+/ATM or pcDNA3.1 zeo+/ATZ,e-qual amount of empty vector was used as control.Cells were treated with NH4Cl for 4 hours and processed for detecting ATZ,LC3 and p62 by immunoblot.Mean-while ,expression and intracellular localization of ATZ, LC3 in 293 T cells were observed with double labeled immunofluorescence.The mRNA levels of autophagy-related genes were measured by real-time PCR.Immu-nohistochemistry was used to observe the morphology of ATZ-positive cells.Results Compared with the control,higher LC3Ⅱ levels and LC3 puncta were observed in ATZ transfected cells.Meanwhile,the levelsof p62 were decreased in ATZ transfected cells,andreversed by NH4 Cl (25 mmol·L -1 )treatment.Overexpression of ATZ increased the mRNA levels of Atg5and Atg12,but had no obvious influence on Beclin1.ATZoverexpressing cells presented abnormal morphologies.The nuclei became reduced,condensed,and even disappeared in ATZpositive cells.Conclusion ATZ overexpression increases autophagy activity whichmay be related to increasing Atg5 and Atg12 levels.

Objective To investigate the effects of phosphocreatine postconditioning on cerebral ischemia-reperfusion(IR)injury in rats.Methods Thirty-six SD rats were randomly divided into three groups:groups Sham,IR (treated with normal saline)and PCr.IR was induced by intraluminal middle cerebral artery occlusion (MCAO).All treatments were given intravenously at the begining of reperfusion.Twenty-four hours after the reperfusion, neurological deficit score and magnetic resonance scan were performed.serum concentrations of malonaldehyde and 4-hydroxynonenal,cere-bral infarct volume and destruction of cerebral cortex were estimated.Neuronal apoptosis was further assessed by immunohistochemistry and immunofluorescent staining of caspase-3 and NeuN. Results Compared with group IR,phosphocreatine significantly decreased neurological deficit score, infarct volume,malonaldehyde and 4-hydroxynonenal levels(P < 0.05 ).Cortex structure was more complete,as well as neuronal apoptotic index was smaller in group PCr (P <0.05).Conclusion PCr can reduce cerebral infarct volume,thereby promote neurofunctional recovery.The mechanism of Pcr is related to reduced oxidative stress and inhibitted apopotosis during IR.

Objective To evaluate the effect of propofol on autophagy during oxygen-glucose deprivation and restoration (OGD/R) in human liver cells.Methods Human hepatic HL-7702 cells at the logarithmic growth phase were seeded into culture plates and randomly divided into 3 groups (n =12 each) using a random number table:control group (group C),OGD/R group,and propofol + OGD/R group (group P+OGD/R).The cells were cultured in normal culture medium in group C.In OGD/R and P+OGD/R groups,the cells were subjected to O2-glucose deprivation for 6 h followed by restoration of O2-glucose supply for 12 h.Propofol with a final concentration of 50 mmol/L was added at 10 min before oxygen-glucose deprivation.The cell viability was detected by MTT assay.The expression of autophagy-related proteins such as microtubule-associated protein light chain 3 (LC3) and Beclin-1 was evaluated by Western blot.Immunofluorescence was used to determine the number and distribution of autophagosomes.Results Compared with group C,the cell viability was significantly decreased,the expression of LC3 and Beclin-1 was significantly up-regulated (P＜0.05),and the number of autophagosomes was significantly increased in OGD/R and P+OGD/R groups.Compared with group OGD/R,the cell viability was significantly increased,the expression of LC3 and Beclin-1 was significantly down-regulated (P＜0.05),and the number of autophagosomes was significantly decreased in group P+OGD/R.Conclusion The mechanism by which propofol reduces OGD/R injury is probably related to inhibition of autophagy in human liver cells.

Purpose To investigate the expression of RNF2 in breast disease tissues and cell lines,and to analyze the association between expression of RNF2 and clinicopathological characteristics in breast carcinoma.Methods Expression of RNF2 protein and mRNA levels was detected using immunohistochemistry of EnVision two-step and qRT-PCR in breast carcinoma and benign breast disease as well as in cell lines.Results RNF2 expression was sigmificantly higher in breast carcinoma tissue specimens compared with benign breast disease specimens (P ＜0.05).Besides,the expression of RNF2 protein was significantly associated to tumor size,lymph node status and TNM stage (P ＜ 0.05 for both),but was not related to age,histological grade,the expression of ER,PR and HER-2 (P ＞ 0.05 for both).Higher expression of RNF2 mRNA was detected in breast carcinoma cell lines compared with breast epithelial cell lines (P ＜ 0.05).Conclusion RNF2 is overexpressed in breast carcinoma and can be a potential therapeutic target for breast carcinoma.

AIM To study the analgesic effects of melatonin (MT) and related mechanisms. METHODS The threshold was measured by hot plate test.? endorphine (? EP) was determined by radioimmunoassay (RIA). RESULTS MT (40～160 mg?kg -1 , ip) had significant dose and time dependent analgesic effects in hot plate test. The analgesia was also induced by injection (icv) of MT (0 25 mg?kg -1 ). The day night rhythm of pain threshold was not observed in 7 d after pinealectomy, but it appeared in sham operated rats.? EP content of rat brain measured by RIA indicated that the level of ? EP in hypothalamus and pituitary decreased significantly 1 h after ip MT(100 mg?kg -1 ). The analgesic effect of MT was attenuated by pretreatment of reserpine (3 mg?kg -1 ip) or ? receptor blocker phentolamine (100 mg?kg -1 , sc). CaCl 2 (230 mg?kg -1 ) antagonized the analgesic effect of MT, and EGTA and verapamil significantly enhanced the analgesia of MT in the same situation. CONCLUSION MT has significant analgesic action which may be related to opiate system, adrenergic system, and Ca 2+ content.

Hypoxia-ischemia induces an inflammatory and immune response in the nervous system that may be important for development of brain injury. Recent data implicate that cytokines, chemokines, adhesion molecules，are involved in the recruitment of inflammatory-immune cells. A cytokines which promote emigration of leukocytes from the vascular lumen into the injured brain tissue are produced at the site of incipient cerebral infarction. The expression of mRNA for alpha- and beta-chemokines preceded the appearance of immune cells suggesting that these molecules may have a role in the inflammatory response to insults. The humoral and cell-medated immunity under the conditions of focal brain ischemia was discussed. These results together indicate that cell-cell interaction by adhesion molecules and cytokines is an important component in the pathogenesis of ischemic cerebral diseases, especially at the acute phase.Recently accumulated data show that depleting the amount of circulating leukocytes or administering anti-inflammatory chemicals such as cytokine blocking agents, anti-adhesion molecule antibodies, and immunosuppressants effectively minimize the size of ischemia induced cerebral infarction.