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Objective To evaluate the cardioprotection of electroacupuncture (EA) in the patients undergoing heart surgery with cardiopulmonary bypass (CPB).Methods Forty American Society of Anesthesiologists physical status Ⅲ patients,aged 18-55 yr,of New York Heart Association Ⅱ-Ⅲ,scheduled for elective cardiac valve replacement with CPB,were divided into 2 groups (n =20 each) using a random number table:control group (group C) and group EA.In group EA,bilateral Neiguan,Ximen,Shenmen and Baihui acupoints were stimulated with an electrie stimulator with the frequency of 2 Hz from 20 min before anesthesia induction until the end of operation,and the optimal intensity was selected according to the patient's tolerance when awake.Before EA and at 30 min of CPB,30 min,1 h and 2 h after termination of CPB and 6 and 24 h after operation,blood samples were taken from the central vein for determination of concentrations of heart-type fatty acid binding protein and cardiac troponin Ⅰ in plasma (by enzymelinked immunosorbent assay) and concentrations of malondialdehyde (using hydroxylamine method).Cardiac contractility was scored at 1,6 and 24 h after operation,and arrhythmia was scored at 24 h after operation.Results Compared with group C,the plasma concentrations of malondialdehyde at 30 min and 1 and 2 h after termination of CPB and 6 h after operation,plasma concentrations of cardiac troponin Ⅰ at 24 h after operation,and plasma concentrations of heart-type fatty acid binding protein at 30 min of CPB and 24 h after operation were significantly decreased,and the arrhythmia score and cardiac contractility score at 6 and 24 h after operation were decreased in group EA (P＜0.05).Conclusion EA can inhibit lipid peroxidation and exerts cardioprotection in the patients undergoing heart surgery with CPB.
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Objective To evaluate the effect of isoflurane preconditioning on the expression of hippocampal GluR1 subunits-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate(AMPA)receptors in a rat model of focal cerebral ischemia-reperfusion(I/R).Methods Forty-eight pathogen-free healthy male Sprague-Dawley rats,weighing 250-280 g,aged 7-8 weeks,were divided into 3 groups(n=16 each)using a random number table:sham operation group(group S),focal cerebral I/R group(group I/R)and isoflurane preconditioning group(group IPC).Focal cerebral I/R was induced by occlusion of the middle cerebral artery for 2 h followed by reperfusion to induce cognitive decline in I/R and IPC groups. Rats were exposed to 1.5% isoflurane for 1 h every day for 5 consecutive days,and the model was established at 24 h after the last exposure in group IPC. Eight rats in each group were selected to perform Morris water maze test for 6 consecutive days starting from 9 or 23 days after operation. The rats were sacrificed at 14 and 28 days after operation,and the hippocampal tissues were obtained for determination of the expression of GluR1 mRNA(by using real-time polymerase chain reaction)and GluR1 protein(by Western blot).Results Compared with group S,the escape latency was significantly prolonged at each time point after operation,the frequency of crossing the original platform quadrant and percentage of swimming distance at the original platform quadrant were decreased at 14 and 28 days after operation,and the expression of GluR1 protein and mRNA was down-regulated at 14 days after operation in I/R and IPC groups(P<0.05).Compared with group I/R,the escape latency was significantly shortened at 10-13 days after operation,the percentage of swimming distance at the original platform quadrant and frequency of crossing the original platform quadrant were increased at 14 days after the operation,and the expression of GluR1 protein and mRNA was up-regulated at 14 days after operation in group IPC(P<0.05).Conclusion The mechanism by which isoflurane preconditioninig improves the cognitive function is related to up-regulation of the expression of hippocampal GluR1 subunits-containing AMPA receptors in a rat model of focal cerebral I/R.
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Objective To evaluate the effect of isoflurane preconditioning on autophagy during focal cerebral ischemia-reperfusion (I/R) injury in rats.Methods Thirty-six healthy male Sprague-Dawley rats,weighing 250-280 g,aged 7-8 weeks,were divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),cerebral I/R group (group I/R) and isoflurane preconditioning group (group IP).Focal cerebral I/R was induced by 2 h middle cerebral artery occlusion followed by 24 reperfusion.Group IP inhaled 1.5％ isoflurane for 1 h per day for 5 consecutive days,the other two groups only inhaled 30％ oxygen,and focal cerebral I/R was induced at 24 h after the last inhalation.At 24 h of reperfusion,neurologic deficit was assessed and scored,the rats were then sacrificed,and brains were removed for determination of cerebral infarct size (using triphenyl tetrazolium chloride staining) and expression of microtubule-associated protein 1 light chain 3-Ⅱ (LC3-Ⅱ) and Beclin-1 (by Western blot).Results Compared with group S,the neurologic deficit scores and cerebral infarct size were significantly increased,and the expression of hippocampal LC3-Ⅱ and Beclin-1 was significantly up-regulated in I/R and IP groups (P＜0.05).Compared with group I/R,the neurologic deficit scores and cerebral infarct size were significantly decreased,and the expression of hippocampal LC3-Ⅱ and Beclin-1 was significantly upregulated in group IP (P ＜ 0.05).Conclusion The mechanism by which isoflurane preconditioning ameliorates focal cerebral I/R injury is related to enhancement of autophagy in the rats.
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Objective To investigate the effect of isoflurane preconditioning on rat learning and memory in cerebral ischemia-reperfusion injury and its possible mechanism.Methods Thirty-six adult male Sprague-Daw ley rats w ere randomly divided into a sham operation group, a cerebral ischemia-reperfusion group, and an isoflurane preconditioning group (n=12 in each group). A model of middle cerebral artery occlusion and ischemic-reperfusion w as induced by a modified intraluminal suture method. The rats of the isoflurane preconditioning group inhaled 1.5%isoflurane for 1 hour per day for 5 d. At 24 h after the last preconditioning, a model of MCAO w as made. At 24 h after MCAO, the infarct volume w as detected by using 2,3,5 chlorinated diphenyl tetrazolium staining. At day 1, 3, 7, and 14 after MCAO, the modified Neurological Severity Score (mNSS) were performed. At day 9 after MCAO, the Morris w ater maze test w as used to evaluate the learning and memory of rats. At day 14, Western blotting w as used to detect the protein expression level of hippocampal tissue glutamate receptor 1 (GluR1) on the side of ischemia. Results No obvious infarcts w ere observed in the rats of the sham operation group. The infarct volume in the isoflurane preconditioning group w as significantly smal er than that of the cerebral ischemia-reperfusion group (26.383%±3.128%vs.19.107%±1.661%;P<0.05). No neurological deficit w as observed in the sham operation group (score 0). The mNSS scores at day 1, 3, 7, and 14 after MCAO in the isoflurane preconditioning group w ere decreased significantly (day 1:9.000 ±1.195 vs.11.500 ±1.414;day 3:6.6250 ±1.407 vs.6.625 ±1.407vs.6.625 ±1.407; day 7: 5.875 ±0.707 vs.7.375 ±1.407; and day 14:3.375 ±1.187 vs.5.125 ±1.246;al P<0.05). The Morris w ater maze show ed that the escape latencies at day 1-5 after MCAO in the isoflurane preconditioning group w ere al significantly shorter than those in the cerebral ischemia-reperfusion group (day 1: 95.992 ±15.734 s vs.103.008 ±11.654 s; day 2: 70.949 ±14.708 s vs. 94.705 ±14.709 s;day 3:39.660 ±7.413 s vs.65.716 ±10.155 s;day 4:22.692 ±5.778 s vs.35.240 ±8.553 s;day 5: 14.906 ±4.336 s vs.22.890 ±10.381 s; al P<0.05). The numbers of crossing platform (4.556 ± 1.333 vs.2.889 ±1.536 ) and the percentages of time spent in the target quadrant ( 33.014%±5.223%vs. 21.978%±6.697%) in the isoflurane preconditioning group w ere significantly increased than in the cerebral ischemia-reperfusion group (al P<0.01). The levels of hippocampal GluR1 protein on the ischemic sides in the sham operation group, ischemia-reperfusion group, and isoflurane preconditioning group w ere 0.871 ±0.153, 0.456 ±0.130, and 0.689 ±0.126, respectively. There w ere significant differences among the 3 groups ( F=18.329, P<0.001) and the isoflurane preconditioning group w as significantly higher than the ischemia-reperfusion group (P<0.05). Conclusions Isoflurane preconditioning can improve the learning and memory in cerebral ischemia-reperfusion in rats, its mechanism may be associated w ith the uprelagating GluR1 expression in the hippocampus.
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Objective To evaluate the role of mitochondrial ATP-sensitive potassium (mitoKATP) channel in mitigation of cerebral ischemia-reperfusion (I/R) injury by isoflurane preconditioning in rats and the relationship with c-Jun N-terminal kinase (JNK) signaling pathway.Methods Thirty-two male Sprague-Dawley rats,weighing 280-320 g,were randomly divided into 4 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,isoflurane preconditioning group (group Ⅰ-pre),and 5-hydroxydecanoate (5-HD,a selective mitoKATP channel antagonist) group.Cerebral I/R was produced by modified 4-vessel technique described by Pulsinelli in anesthetized rats.In group Ⅰ-pre,the rats were exposed to 1.5％ isoflurane for 1 h everyday for 5 consecutive days before ischemia.In group 5-HD,5-HD 15 mg/kg was injected intraperitoneally at 30 min before ischemia and the other procedures were similar to those previously described in group Ⅰ-pre.Neurological behavior was evaluated at 24 h of reperfusion.The rats in each group were sacrificed at 72 h of reperfusion,and the brains were removed for determination of neuronal apoptosis (by TUNEL) and expression of caspase-3 and phosphor-JNK (p-JNK) protein (using Western blot) in hippocampal tissues.Apoptotic rate was calculated.Results Compared with group S,the number of grid cross was significantly decreased,hanging time was shortened,apoptotic rate was increased,and caspase-3 expression was up-regulated in I/R,Ⅰ-pre and 5-HD groups,the expression of p-JNK protein was up-regulated in IR and 5-HD groups,and no significant change was found in the expression of p-JNK protein in group Ⅰ-pre.Compare with group I/R,the number of grid cross was significantly increased,hanging time was prolonged,apoptotic rate was decreased,and the expression of caspase-3 and p-JNK protein was downregulated in group Ⅰ-pre,and no significant change was found in the parameters mentioned above in group 5-HD.Compared with group Ⅰ-pre,the number of grid cross was significantly decreased,hanging time was shortened,apoptotic rate was increased,and the expression of caspase-3 and p-JNK protein was up-regulated in group 5-HD.Conclusion The mitoKATP channel is involved in mitigation of cerebral I/R injury by isoflurane preconditioning through blocking the JNK signaling pathway in rats.
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Objective To profile the phenotype and pathogens of cutaneous and mucous mycoses in a dermatology outpatient clinic in Nanchang region. Methods A review was performed to assess cutaneous and mucous mycoses diagnosed in the dermatology outpatient clinic of Dermatology Hospital of Jiangxi Province from 2006 to 2008. The relationship of clinical phenotype and pathogens to season, patients' age and gender was analyzed. Results A total of 7251 cases were collected, and the ratio of male to female patients was 2.3: 1. The most prevalent mycoses included tinea cruris (2702, 37.1%), pityriasis versicolor (1505, 20.8%) and tinea manus (727, 10.0%). In total, 4953 fungal strains were isolated from all the patients except for those with pityriasis versicolor, of them, Trichophyton rubrum accounted to 69.9%, Candida to 20.4%, and Trichophyton violaceum to 4.5%. Season, patients' age and gender were found to be associated with clinical phenotypes and pathogens of mycoses. Conclusions In the dermatology outpatient clinic of Nanchang region, tinea cruris is the most common superficial fungal disease, with the predominant pathogen being Trichophyton rubrum. Trichophyton violaceum is the primary pathogen of tinea capitis, which is different from other reports.
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Objective To investigate the effects of artesunate on human cervical cancer cell line HeLa.Methods The inhibitory effect on cell proliferation was assessed by MTT assay.Transmission electron microscopy and fluorescent staining were applied to demonstrate the presence of apoptosis.Cell cycle,reactive oxygen species(ROS) levels and mitochondrial membrane potential(??m) were examined by flow cytometry,respectively.Expression of caspase-3 was detected by immunohistochemical methods.Results Growth inhibition of ART on HeLa cells was time-and dose-dependent.Apoptotic feature was observed by transmission electron microscopy and fluorescent staining.The blocking of the cell cycle was in S-phase.The expression of caspase-3 in cytoplasm was positive.The generation of ROS increased obviously(P
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Objective To study the effect of basic fibroblast growth factor (bFGF) on proliferating of rabbit lens epithelial cells(RLECs).Methods The second and three generations of RLECs were exposed to different concentrations of bFGF, and the proliferation characteristics of the cells were measured with methyl thiazolyl tetrazolium (MTT) assay. The ultrastructure of cell were observed with transmission electron microscope (TEM).The changs of cells cycles were observed with flow cytometer (FCM).Results After the treatment of bFGF, RLECs showed the marked proliferation , especially in 10μg*L-1 of bFGF . TEM result showed that the cells were more active with bFGF, FCM result showed that the S phase cell obviously increased.Conclusion bFGF is an important factor that can promote proliferation of RLECs.