Objective To explore the neuroprotective effect and mechanism of picroside II on ERK1/2 signal transduction pathway after cerebral ischemia injury in rats.Methods The focal cerebral is-chemic models were established by inserting a monofilament threads into middle cerebral artery occlusion (MCAO) in 100 Wistar rats and treated by injecting picroside II (20 mg/kg) intraperitoneally.The neu-robehavioral function was evaluated by modified neurological severity score points ( mNSS) test.The cerebral infarct volume was measured by tetrazolium chloride ( TTC) staining.The apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling ( TUNEL) assay.The expression of pERK1/2 in cortex was determined by the immunohistochemistry ( IHC) and Western Blot ( WB) .Results mNSS test showed that severe neurological dysfunction was found in model and LPS groups,and the scores of mNSS were significantly increased;meanwhile the scores of mNSS in treatment group and U0126 group were signifi-cantly lower than that in model and LPS groups (P<0.05).TUNEL assay showed that the apoptotic cell inde-xes (ACI) in different groups were (0.06±0.02),(0.27±0.03),(0.07±0.02),(0.26±0.03)and(0.09± 0.05) ,and the ACI in treatment and U0126 groups was obviously lower than that in model and LPS groups (P<0.05) .With IHC and WB,pERK1/2 level in model group was the highest,which was slightly higher than that of LPS group,and pERK1/2 expression in treatment and U0126 groups was significantly decreased com-pared with that in model and LPS groups (P<0.05) .Conclusion The activation of ERK1/2 by cerebral is-chemia could induce the cell apoptosis.Picroside II might reduce cell apoptosis by inhibiting the activation of ERK1/2 in ischemic brain injury.

Objective To explore the possible effects on differentiation of SHI-1 cells induced by puerariae radix flavones(PRF)in vitro.Methods SHI-1 cells were treated with PRF in various concertration,then the inhibitory effects of cell proliferation were detected by MTT assay,the cell cycles were analyzed by flow cytometry(FCM),the cells reduction rates were detected by NBT reduction test,and the expression of CD11b and CD14 were tested by FCM.Results 10-50 μg/ml PRF could inhibit the proliferation of SHI-1 cells in a time-and dose-dependent manner,and the cell cycles were arrested in S phase.When SHI-1 cells were treated with 10,30 and 50 μg/ml PRF in 48 houres respectively,the NBT reduction rates of cells were increased in a dose-dependent with PRF(P＜0.05),and the expression of cells surface differentiation antigen CD14 was also increased along with the concentration of PRF.Conclusion The SHI-1 cells could be induced to differentiation partially after treated with 10,30 and 50 μg/ml PRF in vitro.

Aim To investigate the neuroprotective effect of picroside Ⅱ(PIC)on cyto C/caspase-9/caspase-3 signal pathway following ischemia/reperfusion(I/R)injury in rats.Methods Atractyloside(Atr)was selected as negative control,cyclosporin A(CsA)was selected as positive control,and PIC was selected as the treatment medicine.The I/R model was made by inserting a monofilament suture into internal carotid artery for 2 h,and then reperfused for 24 h.The cerebral infarction volume was detected by TTC staining,and the expression of cyto C,caspase-9 and caspase-3 were determined by immunohistochemical assay and Western blot.Results In model group,the cerebral infarct volume was obviously large;the expression of cyto C,caspase-9 and caspase-3 was increased significantly more than that in sham group(P<0.05).In PIC group,the cerebral infarct volume was significantly improved;the expression of cyto C,caspase-9 and caspase-3 was significantly decreased than that in model group(P<0.05).In Atr+PIC group,the rat infarction volume was reduced,and the expression of cyto C,caspase-9 and caspase-3 was significantly decreased than that in Atr group(P<0.05).Conclusion The mechanism of PIC inhibiting neuron apoptosis in focal cerebral I/R rats might be through down-regulating the expression of cyto C,caspase-9 and caspase-3.

Objective To explore the clinical characteristics and prognostic factors of primary gastric lymphoma.Methods Clinical data of 78 primary gastric lymphoma patients treated between September 2012 and January 2017 in our hospital were analyzed retrospectively.Results 1-year and 3-year survival rate were 86％ and 68％ respectively.Univariate analysis showed that the four factors including the level of serum lactate dehydrogenase (x2 =35.088,P =0.000),Musshoff stage (x2 =29.930,P =0.000),pathology types (x2 =6.077,P =0.014),IPI score (x2 =21.337,P =0.000) were associated with the prognosis.Multivariate analysis showed that Musshoff stage was an independent risk factor for the prognosis when stage Ⅰ,stage Ⅱ (OR =1.075,95％ CI:0.060-19.107,P =0.961) were compared with stageⅢ (OR =11.994,95％ CI:1.042-138.083,P =0.046),or stage Ⅳ (OR =13.165,95％ CI:1.476-117.417,P =0.021).Conclusions Musshoff stage is an independent factor for the prognosis,surgical treatment can not prolong survival and chemotherapy is the therapy of choice.

Objective To investigate the effect ofpicroside Ⅱ on mitochondria cytochrome C (CytC) expression and its significance in rats after ischemia/reperfusion.Methods Ninety-six Wistar rats were randomly divided into sham-operated group,model group,picroside Ⅱ group,Cyclosporin A (CsA,specific antgonist of CytC) group,CsA+picroside Ⅱ group,atractyloside (Atr,selective agonist of CytC) group,Atr+picroside Ⅱ group and DMSO group (n=12);the middle cerebral artery occlusion/reperfusion models referring to Longa's method with medications were adopted,which were established by inserting a monofilament suture into the internal carotid artery for 2 h and then reperfusion for 24 h.After 24 h of ischemia/reperfusion,modified neurological severity scale (mNSS) scores were observed,contents of reactive oxygen species (ROS) in brain tissues were measured by enzyme-linked immunosorbent assay (ELISA),morphology of brain tissues was observed by hematoxylin-eosin staining,ultrastructures ofmitochondria were observed by transmission electron microscopy,apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling assay (TUNEL),and CytC expression was determined by immunohistochemical assay and Western blotting.Results As compared with the sham-operated group,the model group had significantly increased mNSS scores,ROS contents,number ofapoptotic cells and CytC expression (P＜0.05),and the mitochondria structure was seriously destroyed.The picroside Ⅱ group had obviously decreased mNSS scores,ROS contents,number of apoptotic cells and CytC expression,and the morphology of brain tissue was improved and the mitochondria damage was reduced as compared with the model group,with significant differences (P＜0.05).The Atr+picroside Ⅱ group had significantly decreased mNSS scores,ROS contents,number of apoptotic cells and CytC expression (P＜0.05),and the mitochondria damage in the Atr+picroside Ⅱ group was reduced as compared with that in the Atr group with significant difference (P＜0.05).Conclusion The mechanism of picroside Ⅱ protecting against focal cerebral ischemia reperfusion might attribute to decrease of ROS contents,protection of mitochondria structure and down-regulation of CytC expression in middle cerebral artery occlusion/reperfusion rats.