ABSTRACT
Objective To evaluate the effect of propofol preconditioning on endoplasmic reticulum stress induced by hypoxia-reoxygenation (H/R) in HEPG2 cells.Methods HEPG2 cells were randomly divided into 4 groups using a random number table:control group (group C),propofol group (group P),H/R group and H/R + propofol preconditioning group (group PP).In group C,the cells were cultured routinely for 42 h.In group H/R,after being cultured routinely for 6 h,the cells were exposed to 1％ O2 + 5％ CO2 + 94％ N2 for 12 h followed by 12 h reoxygenation.In group PP,the cells were cultured for 6 h in the culture medium containing propofol 10 μmol/L (final concentration),and then H/R was induced.The cell viability was detected by MTT assay.The expression of immunoglobulin heavy chain-binding protein (BIP),C/EBP homologous protein (CHOP) and activated caspase-3 was determined by Western blot.The expression of BIP,CHOP and caspase-3 mRNA was determined by RT-PCR.Results Compared with group C,the cell viability was significantly decreased,and the expression of BIP,CHOP and activated caspase-3 protein and mRNA was up-regnlated in H/R and PP groups,and no significant changes were found in the parameters mentioned above in group P.Compared with group H/R,the cell viability was significantly increased,and the expression of BIP,CHOP and activated caspase-3 protein and mRNA was down-regulated in PP group.Conclusion Propofol preconditioning can promote the cell proliferation and attenuate H/R injury to HEPG2 cells through inhibiting endoplasmic reticulum stress.
ABSTRACT
Objective To evaluate the effect of propofol on the endoplasmic reticulum stress-mediated apoptosis during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Eighty adult male Sprague-Dawley rats,weighing 240-280 g,were randomly divided into 4 groups (n =20 each):shame operation group (group S) ; focal cerebral I/R group (group FCIR); propofol pretreatment group (group P); intralipid pretreatment group (group Ⅰ).Focal cerebral I/R was induced by 4 h middle cerebral artery occlusion followed by reperfusion.Propofol was infused at a rate of 12 mg· kg-1 · h-1 starting from 30 min before ischemia until 15 min of ischemia in group P,while intralipid was given instead of propofol in group I.Neurological deficit scores (NDSs) were measured at 6 h of reperfusion in 10 rats chosen from each group and the rats were then sacrificed.Their left brains were removed for determination of brain water content.The left 10 rats were sacrificed and their brains were immediately removed for determination of the expression of C/EBP homologous protein (CHOP),Bcl-2,and activated caspase-3 in the left hippocampi by Western blot.Results Compared with group S,NDSs and brain water content were significantly increased,the expression of CHOP and activated caspase-3 was up-regulated,and the expression of Bcl-2 was down-regulated in group FCIR,NDSs was increased in group P (P ＜ 0.05).Compared with group FCIR,NDSs and brain water content were significantly decreased,the expression of CHOP and activated caspase-3 was down-regulated,and the expression of Bcl-2 was up-regulated in group P,and no significant change was found in each parameter in group Ⅰ (P ＞ 0.05).Conclusion Propofol can reduce focal cerebral I/R injury through inhibition of the endoplasmic reticulum stress-mediated apoptosis in rats.
ABSTRACT
Objective To study the effect of synthesized peptide S247 on the activation of p38MAPK of ventilator- induced lung injury.Methods Thirty healthy male SD rats were divided into group A,group B,group C,n 10.All rats were performed with mechanical ventilation,group A with tidal volume(V_T)8 ml/kg,breathing rate(p)80/min;group B with tidal volume(V_T)40 ml/kg,breathing rate(p)=80/min;group C with tidal volume(V_T)40 ml/kg,breathing rate(p)80/min.The rats in group C were intraperitoneally injected with synthesized peptide S247(100 mg/kg)once a day for a week.The time of ventilation in all groups was two hours.Rats were sacrificed after the experiment was finished. The lung lavage liquid and lung tissue were collected and stored with correct methods.The measured indexes included lung pathology change,total protein,WBC,MPO and MIP-2.The expression of p38 and p-p38 were measured by Western Blot in lung tissue.Results Compared with group A,total protein,WBC,MPO,MIP-2 and p-p38 significantly increased in group B;compared with group B,total protein,WBC,MPO,MIP-2 and p-p38 significandy decreased in group C. Conclusion Synthesized peptide S247 significantly inhibited the activation of p38 and relieved the degree of ventilator induced lung injury.
ABSTRACT
Objective To evaluate the expression of ?-defensin-2(BD-2) gene and protein with ventilator-associated pneumonia(VAP) in the old and grown rats.Methods Fifty-eight normal healthy Sprague-Dawley rats were divided into the old group(400～460 g,15～18 months,n=29) and grown group(280～320 g,4～6 months,n=29).Each rat received ventilation(VT=12 ml/kg) through tracheal tube for 24h and was challenged intra-tracheally with Pseudomonas aeruginosa(0.2 ml).The mRNA and protein levels of BD-2 were detected by RT-PCR and Western blot analysis respectively. Results Compared with the grown group,the rats had more severe interstitial pulmonary edema in the old group.There was no dominant difference in BD-2 mRNA and protein expression between the grown group and old group within 3 h,but BD-2 expressions in the grown group were significantly higher at 3 h,6 h,12 h,1 d,2 d and 3 d than those in the old group(P