Objective To discuss the advantage of hispectral index(BIS) monitoring used in gastrointestinal endoscopy,and to observe elinical effects of target-controlled infusion(TCI) propofol combined with remifentanyl in elderly patients.Methods 120 patients aged from 65 to 78 with ASA physical status Ⅰ ～ Ⅱ were randomly divided into two groups,i,e.Group A (propofol with fentanyl ),Group B ( TCI propofol and remifentanyl with BIS).The amount of propofol was adjusted by consciousness and hemodynamics in Group A,while by BIS value in Group B.BIS was controlled at 55 ～60.The total amount of propofol and the time of wake-up,the incidence of complicatiors in each group were recorded.Results Compared with Group A,the changes of MAP and HR at T1 and T2 were smaller in Group B(P ＜ 0.05 ) ; Compared with Group A,the total amount of propofol and the time of wake-up were less in Group B ( P ＜ 0.05 ) ;Compared with Group A,the incidence of intraoperative respiratory depression and bradycardia were increased in Group B( P ＜ 0.05 ),there were no differences in the rest between the two groups.Conclusion Under BIS monitoring,TCl propofol and remifentanyl in elderly patients undewent gastrointestinal endoscopy may reduce propofol,and reach rapid recovery from anesthesia,but it needs additional management of respiration and circulation.

ObjectiveTo observe the changes of HR,MAP,BIS and Narcotrend induced by different doses of propofol in elderly patients. MethodsOne hundred elder patients(60 ～ 85 years old), AS A class Ⅰ or Ⅱ, scheduled for selective surgeries,were divided equally into 5 different doses of propofol( constant intravenous injection for 1min) groups of 0.5mg/kg( Ⅰ ) ,0. 75mg/kg( Ⅱ ) ,1.0mg/kg(Ⅲ) ,1.25mg/kg( Ⅳ)and 1.5mg/kg(Ⅴ). HR,MAP,BIS and Narcotrend were monitored before propofol injection and at 1 and 5 min after propofol injection. ResultsHR of 5 group s as similar. At 1 min after pmpofol injection, MAP decreased remarkably compared with at before in all 5 groups( t =2. 17,2.84,2.49,5.63,7.10, all p ＜ 0.05 ), which in group Ⅳ and Ⅴ decreased significantly compared with at in group Ⅰ, Ⅱ and Ⅲ(t =4.67,2.77,2.45,5.49,4.57,2. 18,all P＜0.05).At 1 min after propofol injection,BIS and NI values decreased compared with at before in all 5 groups(t =7.74,11.74,28.18,30.34,45.28, 6. 65,10.52,17.27,26.28,30. 14,allP ＜0.05) ,which in groupⅢ, Ⅳ and Ⅴ were significantly lower than those in group Ⅰ and Ⅱ (t =12.59,11.08,16.72,15.12,17.67,15.64,allP＜0.05).Dose of propofol was negatively correlated with BIS and NI value ( r =-0. 898/0. 930, P ＜ 0.01 ). ConclusionPropofol 1.0mg/kg constant injection should meet the sedation and hypnosis demand of general anesthesia in elderly patients and could not inhibit circulatory system; Bispectral Index and Narcotrend could accuratly monitor depth of anesthesia in elderly patients.

Objective: To explore the effect of tanshinone IIA on neuronal apoptosis in the compressed spinal cord and its molecular mechanism by establishing a spinal cord compression model. Methods: Twenty-four SD rats weighing 250-300 g were the experimental animals. The spinal cord compression model was established by clamping the spinal cord with arterial clamp. Six rats in each group were randomly selected and randomly divided into sham group (Sham group, given intraperitoneal injection of normal saline at the same dose once a day) and spinal cord compression injury group (SCI group, given normal salts). Water intraperitoneal injection, once a day), tanshinone IIA group (TAN group, 30 mg/kg tanshinone IIA intraperitoneal injection, once a day), LY2904002 group (LY group, 0.3 mg/kg LY294002 intraperitoneal injection, 5 min after 30 mg/kg tanshinone IIA intraperitoneal injection, once 1 d). After 3 d of intervention, the motor function of rats were evaluated by inclined plane test and BBB score. The expression of apoptotic genes and PI3K/AKT signaling molecules in the compressed spinal cord were detected by qPCR, immunohistochemistry and Western blot. Results: The BBB score 3.31±0.45 points, inclined angle 9.31°±1.02°, GSK-3β 0.35±0.06, CyclinD1 0.25±0.06, Bcl-2 0.38±0.06, p-PI3K 0.32±0.05, p-AKT 0.29±0.07 protein expression in SCI group were lower than those in Sham group. The protein expression of Caspase-9 3.27±0.54 and Caspase-3 2.73±0.35 in SCI group was higher than that in Sham group. The BBB score 9.31±1.02 points, inclined angle 24.95°±3.52°, GSK-3β 0.74±0.09, CyclinD1 0.69±0.11, Bcl-2 0.83±0.13, p-PI3K 0.77±0.11, p-AKT 0.69±0.08 in TAN group were higher than those in SCI group BBB score 3.31 ±0.45 points, inclined angle 9.31°±1.02°, GSK-3β 0.35±0.06, CyclinD1 0.25±0.06, Bcl-2 0.38±0.06, p-PI3K 0.32±0.05, p-AKT 0.29±0.07. The protein expression levels of Caspase-9 1.78±0.22 and Caspase-3 1.64±0.2 in TAN group were lower than those in SCI group 3.27±0.54 and Caspase-3 2.73±0.35. The BBB score, oblique angle and the expression of GSK-3β 0.43±0.07, CyclinD1 0.38±0.06, Bcl-2 0.49±0.09 in LY group were lower than those in TAN group. The protein expression of Caspase-9 2.54±0.38 and Caspase-3 2.25±0.37 in LY group were higher than TAN group. Conclusion Tanshinone IIA can inhibit the apoptosis of spinal cord tissue and alleviate the spinal cord injury in spinal cord compression rats by activating the PI3K/AKT signaling pathway.

Objective:To investigate the neuroprotective effect of histone deacetylase 3 (HDAC3) specific inhibitor RGFP966 on traumatic brain injury (TBI) and its mechanism in rats.Methods:Forty-eight SD rats were randomly divided into sham-operated group, TBI group, TBI+vehicle group and TBI+RGFP966 group ( n=12). Rats in the later 3 groups accepted hydraulic impact brain injury to establish TBI models; and then, RGFP966 (dissolved in 1% DMSO at a dose of 10 mg/kg) was injected intraperitoneally 30 min after modeling, twice a day for 3 d, in TBI+RGFP966 group; same amount of DMSO was injected into TBI+vehicle group at the same time. Three d after modeling, neurological function was tested by modified neurological severity score (mNSS), water content of brain tissues was detected by dry-wet weight method, proportion of injured neurons at the frontal cortical tissues on the affected side was detected by Nissl staining, expressions of HDAC3 and pyroptosis related proteins were detected by immunohistochemical staining and Western blotting, and serum content of inflammatory factors was detected by ELISA. Results:Three d after modeling, compared with the TBI+vehicle group, the TBI+RGFP966 group had significantly decreased mNSS scores (9.83±0.75 vs. 6.67±0.82), water content of the injured cerebral cortex (82.73%±0.36% vs. 80.92%±0.66%), proportion of damaged neurons (75.60%±7.44% vs. 55.87%±4.10%), and HDAC3 protein expression (0.67±0.09 vs. 0.51±0.07), and significantly increased acetylated H3 (Ace-H3) and acetylated H4 (Ace-H4) protein expressions (0.81±0.02 vs. 1.22±0.02; 0.74±0.01 vs. 1.07±0.02), and statistically decreased protein expressions of nuclear factor-κB (NF-κB, 1.20±0.05 vs. 0.94±0.04), NOD-like receptor thermal protein domain associated protein 3 (NLRP3, 0.72±0.02 vs. 0.40±0.03), Caspase-1 containing cysteine (Caspase-1), dermatin D N-terminal fragment (GSDMD-N, 0.71±0.03 vs. 0.52±0.01), significantly decreased NF-κB and NLRP3 immunohistochemical staining scores, and significantly decreased serum contents of tumor necrosis factor-α, interleukin(IL)-1β and IL-18 ( P<0.05). Conclusion:Early intervention with RGFP966 after TBI can reduce the pyroptosis and inflammatory reaction of nerve cells and play neuroprotective role, whose mechanism may be related to inhibited activation of NF-κB/NLRP3/GSDMD pathway.

Background It has been found that fluoride may cause cardiomyocyte damage. c-Jun N-terminal kinases (JNK) signaling pathway plays an important role in apoptosis, but its role in fluorosis-induced cardiomyocyte damage is still unknown yet. Objective To explore the toxic effect of sodium fluoride (NaF) on H9c2 cardiomyocytes of rats and whether NaF affects cardiomyocyte apoptosis through the JNK signaling pathway. Methods According to the concentrations of sodium fluoride and whether sp600125 (JNK inhibitor) was added, cardiomyocytes of rats were divided into six groups, including control group, SP600125 group (SP group), 0.24, 0.48, and 0.96 mmol·L⁻¹ NaF groups, and 0.96 mmol·L⁻¹ NaF+SP600125 group (NaF+SP group). Cardiomyocytes exposed to NaF for 24 h were observed using a fluorescence inverted microscope. The changes of cell viability at 24, 48, and 72 h after the treatment were detected by CCK-8 method. The levels of reactive oxygen species (ROS) at 24 h after the treatment in H9c2 cardiomyocytes were determined by fluorescent probe method. The expression levels of Bcl-2, Bax, Caspase-3, and JNK mRNA at 24 h after the treatment were detected by real-time PCR. The protein expression levels of Bcl-2, Bax, Caspase-3, and p-JNK at 24 h after the treatment were detected by Western blotting. Results Compared with the control group, after being exposed to 0.48 and 0.96 mmol·L⁻¹ NaF for 24 h, the cell growth density decreased. With the increase of NaF concentration, rounded cells and some suspended dead cells appeared. At 24h after exposure to NaF, the cell viability of the 0.48 and 0.96 mmol·L⁻¹ NaF groups decreased compared with the control group (P<0.05). At 48h and 72h after exposure to NaF, the cell viability levels of the NaF treated groups were significantly lower than that of the control group (P<0.05). After NaF exposure for 24 h, compared with the control group, the intracellular ROS levels were increased (P<0.05); the mRNA expression levels of Bcl-2 were decreased to varying degrees, especially in the 0.48 and 0.96 mmol·L⁻¹ NaF groups (P<0.05); the mRNA expression levels of Bax, Caspase-3, and JNK were increased (P<0.05); the protein expression levels of Bcl-2 were reduced (P<0.05); the protein expression levels of Bax, Caspase-3, and p-JNK were elevated (P<0.05). Compared with the 0.96 mmol·L⁻¹ NaF group, the cell viability of the NaF+SP group was increased, the intracellular ROS level was decreased, the mRNA expression levels of Bax, Caspase-3, and JNK were decreased, the protein expression level of Bcl-2 was increased, and the protein expression levels of Bax, Caspase-3, and p-JNK were decreased (P<0.05); the expression level of Bcl-2 mRNA had a rising trend but showed no statistical significance (P>0.05). Conclusion Cardiomyocyte damage after excessive fluoride exposure may result from fluoride inducing excessive ROS production in cardiomyocytes, which may activate the JNK signaling pathway and induce cardiomyocyte apoptosis.

Objective : To investigate the effect of hypoxic preconditioning (HPC) on mitochondrial energy metabolism in mouse hippocampal HT22 cells and its possible mechanism. Methods : In this paper, mouse hippocampal nerve cells HT22 were divided into control group, hypoxia group, HPC group, and the levels of adenosine triphosphate (ATP) and reactive oxygen species (ROS) in each group were measured for observing the effect of HPC on cell mitochondrial metabolism. Western blot was used to detect the expression of target of rapamycin ( mTOR), phosphorylated mTOR protein and autophagy substrate P62 protein; cellular immunofluorescence was used to detect phosphorylated mTOR, and LysoTrackerTM probe was used to detect lysosomes. Results : Compared with the control group, the ATP level was significantly decreased and the ROS level was increased in the hypoxia group. Exposed to HPC, the ATP level was increased and the ROS level was decreased. Compared with the control group, the expression of phosphorylated mTOR was down⁃regulated and the expression of autophagy substrate P62 was down⁃regulated in the HPC group. Conclusion HPC may affect the energy metabolism of HT22 cells through the mTOR/autophagy signaling pathway, thereby exerting a protective effect on the HT22 cells.