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Objective:To evaluate the effect of intra-articular injection of different concentrations of ozonated water on articular cartilage of rabbits with osteoarthritis (OA).Methods:Twenty-four clean-grade New Zealand white rabbits of both sexes, weighing 2.0-3.0 kg, aged 6 months, were divided into 4 groups ( n=6 each) using a random number table method: control group (group C), OA group, low concentration ozonated water group (L group) and high concentration ozonated water group (H group). The OA model was established by intra-articular injection of papain.At 2 weeks after the model was successfully established, 10.0 and 20.0 μg/ml ozonated water 1.0 ml was injected into the knee joint of rabbits in L and H groups, respectively, and 0.9% sodium chloride solution 1.0 ml was injected once a week, 3 times in total in OA group.At 1 week after the last injection, the cartilage tissue of the knee joint was removed and stained with toluidine blue for evaluation of Mankin score (under light microscope). The activity of caspase-3 in chondrocyte was detected by enzyme-linked immunosorbent assay. Results:Compared with group C, the Mankin score and caspase-3 activity were significantly increased in the other 3 groups ( P<0.05). Compared with group OA, the Mankin score and caspase-3 activity were significantly decreased in group L and group H ( P<0.05). Compared with group L, the Mankin score was significantly increased, and the activity of caspase-3 was decreased in group H ( P<0.05). Conclusion:Injecting ozonated water 10.0 μg/ml and 20.0 μg/ml into the knee joint cavity both can inhibit the apoptosis in chondrocytes and reduce the damage to articular cartilage, however, high concentration of ozonated water can cause the denaturation of the articular cartilage matrix in rabbits with OA.
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Objective:To evaluate the effect of orexin-A on programmed necrosis during cerebral ischemia-reperfusion (I/R) in rats.Methods:Thirty clean-grade healthy adult male Spraugue-Dawley rats, weighing 280-320 g, were divided into 3 groups ( n=10 each) using a random number table method: sham operation group (Sham group), cerebral I/R group (I/R group) and orexin-A group (OA group). In I/R and OA groups, a rat model of global cerebral I/R injury was established by transesophageal cardiac pacing-induced cardiac arrest and cardiopulmonary resuscitation in anesthetized animals.Orexin-A 30 μg/kg (diluted to 0.5 ml in phosphate buffer solution) was intravenously injected at 10 min before establishing the model in OA group.Phosphate buffer solution 0.5 ml was intravenously injected at 10 min before establishing the model in Sham and I/R groups.The neurological deficit score (NDS) was assessed at 24 h of reperfusion, then the rats were sacrificed, and bilateral hippocampal tissues were obtained.The morphological structure of pyramidal cells in the hippocampal CA1 region was examined after HE staining, and normal pyramidal cells were counted.Western blot was used to detect the expression of receptor-interacting protein 1 (RIP1), RIP3 and mixed-lineage kinase domain-like protein (MLKL). Immuno-histochemistry was used to count RIP1, RIP3 and MLKL positive cells in the hippocampal CA1 region.The activity of superoxide dismutase (SOD) in hippocampi was determined by xanthine oxidase method, and the content of malondialdehyde (MDA) in hippocampi was determined by thiobarbituric acid method. Results:Compared with Sham group, the normal pyramidal cell count in the hippocampal CA1 region was significantly decreased, NDS was increased, the expression of RIP1, RIP3 and MLKL protein was up-regulated, the positive cell count was increased, the content of MDA in hippocampi was increased, and the activity of SOD in hippocampi was decreased in I/R and OA groups ( P<0.05). Compared with I/R group, the count of normal pyramidal cells in the hippocampal CA1 region was significantly increased, NDS was decreased, the expression of RIP1, RIP3 and MLKL protein was down-regulated, the count of positive cells was decreased, the content of hippocampal MDA was decreased, and the activity of hippocampal SOD was increased in OA group ( P<0.05). Conclusion:The mechanism by which orexin-A reduces cerebral I/R injury may be related to inhibiting programmed necrosis in rats.
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Objective To evaluate the role of nuclear factor erythroid 2-related factor 2 ( Nrf2 ) signaling pathway in endoplasmic reticulum stress response during lipopolysaccharide ( LPS)-induced acute lung injury ( ALI) in mice. Methods Forty clean-grade healthy male C57BL∕6 mice, aged 6-8 weeks, weighing 22-26 g, were divided into 4 groups ( n=10 each) using a random number table method: control group ( group C) , group ALI, salubrinal group ( group S) and salubrinal plus brusatol group ( group S+B) . Animals were intratracheally instilled with 5 mg∕kg of LPS diluted in normal saline to establish the model of ALI. Animals were intratracheally instilled with 100 μl of normal saline in group C. Mice in group S were intraperitoneally injected with endoplasmic reticulum stress response inhibitor 1 mg∕kg salubrinal at 1 and 24 h after LPS instillation. Mice of group S+B were intraperitoneally injected with brusatol 2 mg∕kg once every other day for 10 days prior to LPS instillation, and the other treatments were similar to those previously de-scribed in group S. Mice were sacrificed at 48 h after LPS administration, and lungs were removed for mi-croscopic examination of the pathological changes of lung tissues which were scored and for determination of contents of IL-17A, tumor necrosis factor-alpha ( TNF-α) and interleukin-6 ( IL-6) in lung tissues ( by en-zyme-linked immunosorbent assay) and expression of Nrf2, CCAAT∕enhancer-binding protein homologous protein (CHOP) and caspase-12 in lung tissues (by Western blot). Lung water content was calculated. Results Compared with group C, the lung water content and contents of IL-17A, TNF-α and IL-6 were significantly increased, the expression of CHOP and caspase-12 in cytoplasma was up-regulated, and the ex-pression of Nrf2 in nuclei was down-regulated in ALI and S+B groups, and the lung water content and con-tents of IL-17A, TNF-α and IL-6 were significantly increased, the expression of Nrf2 in nuclei and CHOP in cytoplasma was up-regulated, and the expression of caspase-12 was down-regulated in group S ( P<0. 05) . Compared with group ALI, the lung water content and contents of IL-17A, TNF-α and IL-6 were significantly decreased, the expression of CHOP and caspase-12 in cytoplasma was down-regulated, the ex-pression of Nrf2 in nuclei was up-regulated ( P<0. 05) , and the pathological changes were significantly at-tenuated in group S. Compared with group S, the lung water content and contents of IL-17A, TNF-α and IL-6 were significantly increased, the expression of CHOP and caspase-12 in cytoplasma was up-regulated, the expression of Nrf2 in nuclei was down-regulated ( P<0. 05) , and the pathological changes of lung tis-sues were accentuated in group S+B. Conclusion Nrf2 signaling pathway is involved in the process of en-doplasmic reticulum stress response during LPS-induced ALI in mice.
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Objective To evaluate the development of cerebral anoxia during controlled hypoten-sion with nicardipine or urapidil after carotid endarterectomy in patients. Methods Forty-four patients of either sex, aged 48-64 yr, scheduled for elective carotid endarterectomy under general anesthesia, requi-ring controlled hypotension after operation, were divided into nicardipine group ( group N ) and urapidil group ( group U) using a random number table method, with 22 patients in each group. Nicardipine at 2. 5μg·kg-1 ·min-1 was intravenously infused in group N, and urapidil 2μg·kg-1 ·min-1 was intravenously infused in group U. After systolic blood pressure was decreased to 130-140 mmHg, the consumption of nicardipine was adjusted to 0. 2 - 0. 5 μg·kg-1 ·min-1 and the consumption of urapidil to 1-2μg·kg-1 ·min-1 in group N and group U, respectively, to maintain systolic pressure at 130-140 mmHg. Heart rate ( HR) , cardiac index ( CI) , bispectral index ( BIS) value, regional cerebral oxygen saturation (rSO2) and end-tidal pressure of carbon dioxide (PETCO2) were recorded after entering the operating room ( baseline) , at the beginning of controlled hypotension ( T1 ) , and at 5, 10, 20, 30, 60 and 120 min af-ter systolic blood pressure was decreased to the target hypotension ( T2-7 ) . Development of cerebral anoxia( the relative decrease in rSO2>12％ of the baseline value) was recorded in controlled hypotension period. Results Compared with the value at T1 , the HR at T2,3 and CI at T3-7 were significantly increased ( P<0. 05), and no significant change was found in rSO2, PETCO2 or BIS value at the other time points in group N (P>0. 05), and rSO2 was significantly decreased at T3-7 (P<0. 05), and no significant change was found in HR, CI, PETCO2 or BIS value at the other time points in group U (P>0. 05). Compared with group N, the HR at T2,3, CI at T3-7 and rSO2 at T3-7 were significantly decreased in group U (P<0. 05). The incidence of cerebral anoxia was significantly higher in group U than in group N ( P<0. 05) . Conclu-sion Controlled hypotension with nicardipine is recommended after carotid endarterectomy in order to avoid the development of cerebral anoxia in the patients.
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Objective To evaluate the effect of ulinastatin on programmed necrosis in hippocampal neurons in a rat model of global cerebral ischemia-reperfusion (I/R).Methods Forty-eight clean-grade healthy adult male Sprague-Dawley rats,aged 8 weeks,weighing 280-320 g,were divided into 3 groups (n=16 each) using a random number table method:sham operation group (Sham group),global cerebral I/R group (I/R group) and ulinastatin group (UT group).Global cerebral I/R was produced by 4-vessel occlusion method in chloral hydrate-anesthetized rats in I/R and UT groups.Ulinastatin 100 000 U/kg was injected via the tail vein at the onset of ischemia in group UT,and the equal volume of normal saline was given instead in Sham and I/R groups.Neurological deficit score (NDS) was estimated at 6,12 and 24 h of reperfusion.Animals were sacrificed at 24 h of reperfusion,brains were removed and the hippocampi were obtained for examination of pathological changes (with a light microscope) and for determination of the malondialdehyde (MDA) content and superoxide dismutase (SOD) activity (by spectrophotometry),and expression of receptor-interacting protein kinase 1 (RIPK1),RIPK3,and mixed lineage kinase domain-like protein (MLKL) in hippocampal tissues (by Western blot).Results Compared with Sham group,the NDS was significantly increased at each time point,the MDA content was increased,the SOD activity was decreased,and the expression of RIPK1,RIPK3 and MLKL was up-regulated in I/R and UT groups (P＜ 0.05).Compared with I/R group,the NDS was significantly decreased at each time point,the MDA content was decreased,the SOD activity was increased,and the expression of RIPK1,RIPK3 and MLKL was down-regulated in UT group (P＜0.05).The pathological changes of hippocampi were significantly attenuated in UT group when compared with I/R group.Conclusion The mechanism by which ulinastatin ameliorates global cerebral I/R injury is related to inhibiting programmed necrosis in hippocampal neurons of rats.
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Objective To evaluate the effect of pulsed radiofrequency (PRF) on spinal adenosine triphosphate (ATP)-P2X4-NLRP3 signaling pathway in rats with neuropathic pain.Methods Forty healthy clean-grade adult male Sprague-Dawley rats,aged 2-3 months,weighing 220-260 g,were divided into 4 groups (n =10 each) using a random number table method:sham operation group (group S),neuropathic pain group (group NP),sham PRF group (group SPRF) and PRF group.Neuropathic pain was induced by chronic constriction injury to the left sciatic nerve of anesthetized rats.Rats received PRF treatment on 7th day after establishing the model in group PRF.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before establishing the model (T0) and at 3,7,10,14,21 and 28 days after establishing the model (T1-6).The rats were then sacrificed and the spinal cord was removed for determination of P2X4 and NLRP3 expression (by Western blot) and interleukin-1beta (IL-1β),IL-2,IL-6 and tumor necrosis factor-alpha (TNF-α) contents (by enzymelinked immunosorbent assay).Results Compared with group S,the MWT and TWL were significantly decreased at T1-6,the expression of P2X4 and NLRP3 was up-regulated,and the contents of IL-1β,IL-2,IL-6 and TNF-α were increased in NP,SPRF and PRF groups (P＜0.05).Compared with group NP and group SPRF,the MWT and MWT were significantly increased at T3-6,the expression of P2X4 and NLRP3 was down-regulated,and the contents of IL-1 β,IL-2,IL-6 and TNF-α were decreased in group PRF (P＜0.05).Conclusion The mechanism by which PRF alleviates neuropathic pain is related to inhibiting ATP-P2X4-NLRP3 signaling pathway in rats.
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Objective To study the effect of sufentanil combined with nalbuphine on patient-controlled intravenous analgesia (PCIA)management after cesarean section.Methods The obj ects of study included 150 primiparas who underwent cesarean section in our hospital from January 2016 to March 2017,aged 20-35 years,weighing 54-89 kg,ASA physical status Ⅰ or Ⅱ.The primiparas were randomly divided into three groups,50 in each group.Sufentanil group (group S):sufentanil 2 μg/kg+tropisetron 10 mg;Nalbuphine group (group N):nalbuphine 2 mg/kg+tropisetron 10 mg;Sufentanil combined with nalbuphine group (group SN):sufentanil 1 μg/kg+nalbuphine 1 mg/kg+tropisetron 10 mg.The VAS scores,Ramsay scores and the incidence of respiratory depression of pain (rest,coughing)and Ramsay sedation scores were observed at 1,3,6,9,12,24,36 h after the caesarean section.Actual pressing times of PCIA were further evaluated.Adverse reactions were ob-served,such as nausea and vomiting,respiratory depression.Results There was no statistical differ-ence in VAS scores,Ramsay scores and the incidence of respiratory depression of patients at rest a-mong the three groups.However,when coughing,the VAS scores in patients of group SN were sig-nificantly lower than those of groups S and N (P<0.05).The incidence of nausea and vomiting in group N and group SN was significantly lower than that in group S (P<0.05).The actual pressing times of PCIA were significantly less in group SN than those in group S and group N (P<0.05). Conclusion Sufentanil combined with nalbuphine can achieve satisfactory analgesic effect on PCIA management after cesarean section.
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Objective To investigate the effect of dexmedetomidine on activations of pulmonary extracellular signal-regulated kinase 1/2 (ERK 1/2 )and serine-threonine kinase (Akt) during isolated lung ischemia-reperfusion injury (LIRI)in rats.Methods Forty-five adult male Spra-gue-Dawley rats were randomly divided into three groups (n=1 5 each):control group (group C),is-chemia-reperfusion group (group IR)and dexmedetomidine group (group DEX).Isolated rat lungs were maintained for normal physical activity,and only received ventilation and perfusion for 150 min in the IL-2 ex-vivo lung perfusion system in group C.Isolated rat lungs were subjected to 60 min of is-chemia and apnea followed by 75 min reperfusion and ventilation 15 min after perfusion in the IL-2 ex-vivo lung perfusion system in groups IR and DEX.Dexmedetomidine with a dose of 10 nmol/L was ad-ministrated into perfusion fluid at the onset of reperfusion in group DEX,and the same volume of saline was injected when perfusion for 75 min and at the onset of reperfusion in groups C and IR,respectively.Patho-logical changes of lungs were examined and the injured alveolus rate (IAR)was counted under light micro-scope.The expression levels of ERK 1/2 or Akt mRNA and phosphorylate-ERK 1/2 (p-ERK 1/2 )or phosphorylate-Akt (p-Akt)protein of lung tissue were tested by reverse transcription-polymerase chain re-action (RT-PCR)and Western blot,respectively.Results Compared with group C,the IAR and the ex-pression levels of ERK 1/2 and Akt mRNA or p-ERK 1/2 and p-Akt protein in lung tissue were high-er in groups IR and DEX (P<0.05).Compared with group IR,the IAR and the expression levels of ERK 1/2 and Akt mRNA or p-ERK 1/2 and p-Akt protein in lung tissue were lower in group DEX (P<0.05).Conclusion Dexmedetomidine may reduce LIRI in rat isolated lungs via inhibiting the expressions of IL-6 and IL-8,and the mechanism may be related to suppressing activations of ERK 1/2 and Akt.
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Objective To investigate the effects of perioperative parecoxib sodium on serum surfactant protein A and inflammatory response in elderly patients undergoing video-assisted thoracoscopic pneumonectomy,Methods Sixty-two ASA Ⅰ or Ⅱ elderly patients,aged 65-78 years,weighing 51-79 kg,scheduled for elective video-assisted thoracoscopic pneumonectomy under general anesthesia,were randomly divided into 3 groups:0.3 mg/kg parecoxib sodium group (group P1,n=21),0.6 mg/kg parecoxib sodium group (group P2,n =21) and control group (group C,n =20).The patients were given intravenous parecoxib sodium of 0.3 mg/kg immediately before induction of anesthesia and at 12 h after operation in group P1,and also parecoxib sodium of 0.6mg/kg immediately before induction of anesthesia and at 12 h after operation in group P2,while the equal volume of normal saline was given in group C.Blood samples were taken from the central vein before the induction of anesthesia(T0),after operation(T1),12 h after operation(T2) and 24 h after operation(T3).The concentration of serum surfactant protein A (SP-A),TNF-α,IL-6 and IL-8 were determined by ELASA.The incidence of pulmonary complications at 72 h after operation were also recorded.Results Compared with T0,the concentration of serum SP-A,TNF-α,IL-6 and IL-8 increased significantly in all groups at T1-T3 (P＜0.05).Compared with C group,the concentration of serum SP-A,TNF-α,IL-6 and IL-8 in groups P1 and P2 decreased significantly at T1-T3 (P＜0.05),there were no significant differences between groups P1 and P2.The incidence of postoperative pulmonary complications had no statistically significant differences between the three groups.Conclusion Parecoxib sodium can significantly reduce the concentration of serum SP-A and alleviate the inflammatory response in elderly patients undergoing video-assisted thoracoscopic pneumonectomy.
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Objective To evaluate the effect of prostaglandin E1 (PGE1) on propofol-induced neuroapoptosis in hippocampus of newborn rats.Methods Thirty-six clean-grade healthy newborn SpragueDawley rats,aged 7 days,weighing 11-16 g,were divided into 3 groups (n=12 each) using a random number table method:control group (group C),propofol group (group P) and group PGE1.Propofol 75 mg/kg was intraperitoneally injected once every other day for 7 consecutive days in P and PGE1 groups.PGE1 10 μg/kg was injected via the tail vein at 30 min before each injection of propofol in group PGE1.Normal saline 3 ml/kg was intraperitoneally injected once every other day for 7 consecutive days in group C.The rats were sacrificed at 60 min after emergence from the last injection.The hippocampi were harvested for determination of neuroapoptosis (by TUNEL),expression of caspase-3,Bcl-2 and Bax (by Western blot),and contents of intedeukin-1bota (IL-1β),IL-6 and tumor necrosis factor-alpha (TNF-α) (by enzyme-linked immunosorbont assay).Results Compared with group C,the contents of hippocampal IL-1β,IL-6 and TNF-α were significantly increased,apoptosis index was increased,the expression of caspase-3 and Bax was up-regulated,and the expression of Bcl-2 was down-regulated in P and PGE1 groups (P＜0.05).Compared with group P,the contents of hippocampal IL-1β,IL-6 and TNF-α were significantly decreased,apoptosis index was decreased,the expression of caspase-3 and Bax was down-regulated,and the expression of Bcl-2 was up-regulated in group PGE1 (P＜0.05).Conclusion PGE1 can reduce propofol-induced neuroapoptosis in hippocampus of newborn rats,and the mechanism may be related to inhibiting inflammatory responses of the hippocampus.
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Objective To evaluate the effect of penehychdine hydrochloride pretreatment on nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway during myocardial ischemia-reperfusion (Ⅰ/R) in rats.Methods Thirty-six clean-grade healthy male Sprague-Dawley rats,aged 2-3 months,weighing 220-240 g,were divided into 3 groups (n=12 each) using a random number table method:sham operation group (group S),myocardial Ⅰ/R group and penehyelidine hydrochloride pretreatment group (group PHC).Myocardial Ⅰ/R was induced by occlusion of the anterior descending branch of left coronary artery for 30 min followed by 120 min reperfusion.At 30 min before ischemia,penehyelidine hydrochloride 2 mg/kg was injected intraperitoneally in group PHC,and the anterior descending branch of left coronary artery was only exposed but not ligated in group S.Rats were sacrificed at the end of reperfusion,and hearts were removed for measurement of the myocardial infarct size (by 2,3,5-triphenyltetrazolium chloride staining),cell apoptosis (by TUNEL) and expression of Nrf2,heme oxygenase-1 (HO-1),NQO1 and γ-glutamylcysteine synthetase (γ-GCS) protein and mRNA (by using Western blot or real-time fluorescence quantitative polymerase chain reaction).The percentage of myocardial infarct size and apoptosis index were calculated.Results Compared with group S,the percentage of myocardial infarct size and apoptosis index were significantly increased,and the expression of Nrf2,HO-1,NQO1 and γ-GCS protein and mRNA was down-regulated in Ⅰ/R and PHC groups (P＜0.05).Compared with group l/R,the percentage of myocardial infarct size and apoptosis index were significantly decreased,and the expression of Nrf2,HO-1,NQO1 and γ-GCS protein and mRNA was up-regulated in group PHC (P＜0.05).Conclusion Penehyclidine hydrochloride pretreatment attenuates myocardial Ⅰ/R injury through activating Nrf2-ARE signaling pathway in rats.
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Objective To evaluate the role of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in remote ischemic preconditioning-induced reduction of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.Methods Sixty-eight healthy male C57BL/6 mice,aged 6-8 weeks,weighing 22-26 g,were divided into 4 groups (n =17 each) using a random number table:control group (group C),ALI group,remote ischemic preconditioning group (group RIPC) and brusatol plus remote ischemic preconditioning group (group B+RIPC).Normal saline 100 μl was intratracheally instilled in group C.ALI was induced by intratracheal instillation of LPS 5 mg/kg in group ALI.Mice in group RIPC were subjected to 6 cycles of 5-min ischemia followed by 5-min reperfusion in the right hindlimbs using a tourniquet,and 1 h later the model of ALI was established.Nrf2 inhibitor brusatol 2 mg/kg (in 100 μl of 1％ dimethyl sulfoxide) was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model in group B.Brusatol 2 mg/kg was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model,and remote ischemic preconditioning was performed at 1 h before establishment of the ALI model in group B+RIPC.Seven mice in each group were selected at 24 h after establishment of the ALI model,and bronchoalveolar lavage fluid (BALF) was collected for determination of protein concentrations and neutrophil count.Mice were then sacrificed and lungs were removed for determination of lung water content,myeloperoxidase (MPO) activity,contents of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α),and expression of Nrf2,HO-1 and high-mobility group box 1 protein (HMGB1) in lung tissues (by Western blot) and for examination of pathological changes (with a light microscope).Results Compared with group C,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,and the expression of Nrf2,HO-1 and HMGB1 was up-regulated in group ALI (P＜ 0.05).Compared with group ALI,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly decreased,the expression of Nrf2 and HO-1 was up-regulated,and the expression of HMGB1 was down-regulated (P＜0.05),and the pathological changes were significantly attenuated in group RIPC.Compared with group RIPC,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,the expression of Nrf2 and HO-1 was down-regulated,and the expression of HMGB1 was up-regulated (P＜0.05),and the pathological changes were aggravated in group B+RIPC.Conclusion The activation of Nrf2/HO-1 signaling pathway is involved in remote ischemic preconditioning-induced reduction of LPS-induced ALI in mice.
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Objective To evaluate the role of protein kinase C in the maintenance of chronic inflammatory pain in rats and the relationship with the expression of Nav1.8 in the dorsal root ganglion (DRG).Methods Thirty pathogen-free healthy female Sprague-Dawley rats,weighing 180-220 g,were divided into 3 groups using a random number table:control group (group C),chronic inflammatory pain group (group CIP) and PKC inhibitor group (group P).Normal saline 20 μl was injected into the plantar surface of the right hindpaw every day for 14 consecutive days in group C.Prostaglandin E2 100 ng was injected into the plantar surface of the right hindpaw every day for 13 consecutive days to establish the model of chronic inflammatory pain,and dimethyl sulfoxide 20μl was injected into the plantar surface of the right hindpaw on 14th day in group CIP.Prostaglandin E2 100 ng was injected into the plantar surface of the right hindpaw every day for 13 consecutive days,and PKC inhibitor GF1O9203X 100 nmol/20 μl was injected into the plantar surface of the right hindpaw on 14th day in group P.The mechanical paw withdrawal threshold (MWT) was measured at 1 day before injection (T0) and 1,3,7 and 14 days after the last injection (T1-4).The DRGs of the lumbar segment (L4.5) were removed for determination of Nav1.8 expression using immunofluorescence and Western blot.Results Compared with group C,the MWT was significantly decreased at T1-4 in CIP and P groups,and the expression of Nav1.8 in DRGs was significantly up-regulated in group CIP (P＜0.05).Compared with group CIP,the MWT was significantly increased at T4,and the expression of Nav1.8 in DRGs was down-regulated in group P (P＜0.05).Conclusion Up-regulated expression of Nav1.8 after PKC activation in DRGs is involved in the maintenance of chronic inflammatory pain in rats.
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Objective To investigate the effect of Kinesio Taping on interleukin-1β(IL-1β),tumor necrosis factor α(TNF-α)and matrix metalloproteinase-3 (MMP-3)in synovial fluid of patients with knee osteoarthritis in early and middle stage.Methods A total of 84 patients with knee osteoarthritis who met the inclusion/exclusion criteria were randomly selected and divided into the control group treated with placebo(kinesiology tape without elasticity)and the experimental group treated with Kinesio Tape.Both two tapes were changed every two days,with 15 times of changes as a course of treatment.Synovial fluid sample was drawn before and one week after treatment,and was used for measuring Levels of 1L-1β,TNF-α and MMP-3 by enzyme-linked immunosorbent assay (ELISA).and knee function was evaluated before and 1 week after treatment.Results Compared with pre-treatment,the levels of IL-1β,TNF-α and MMP-3 in synovial fluid were significantly decreased in the experimental group after treatment [(20.07 ± 6.94) ng/Lvs.(38.12 ± 5.93) ng/L,(42.42±8.76)ng/Lvs.(58.23±9.54)ng/L,(11.28±1.99)μg/L vs.(15.67±2.21)μg/L,t =12.81,7.91 and 9.57,all P＜0.05].The levels of IL-1β,TNF-α and MMP-3 in synovial fluid were lower in the experimental group after treatment than before treatment[(20.07±6.94)ng/L vs.(38.12±5.93)ng/L,(42.42±8.76)ng/L vs.(58.23±9.54)ng/L,(11.28 ±1.99)μg/L vs.(15.67±2.21)ng/L,t =12.81,7.91 and 9.57,all P＜0.05],and were lower in the experimental group after treatment than in control after treatment[(20.07±6.94)ng/L vs.(37.97±6.21)ng/L,(42.42±8.76)ng/L vs.(57.04 ±8.73)ng/L,(11.28± 1.99)μg/Lvs.(15.01± 2.56)μg/L,t =12.46,7.66 and 7.46,all P＜0.05]Lysholm score was significantly higher in the experimental group after treatment than before treatment[(74.5 ± 2.6) vs.(44.7 ± 2.8),t =50.54,P ＜0.05],and was also higher in the experimental group after treatment than in the control group after treatment[(74.5±2.6) vs.(50.2± 2.3),t =45.37,P＜0.05].Conclusions Kinesio Taping can significantly reduce the levels of IL-1β,TNF-α and MMP-3 in synovial fluid of patients with knee osteoarthritis through inhibiting the inflammatory response in articular cavity.
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Objective To evaluate the effect of high-level spinal cord injury(SCI)on the expression of mitochondrial voltage-dependent anion channel 2(VDAC2)in rat cardiomyocytes.Methods Forty-eight pathogen-free healthy adult male Sprague-Dawley rats,weighing 200-250 g,were divided into 2 groups(n=24 each)using a random number table:sham operation group(group S)and high-level SCI group(group H).The animals were anesthetized with intraperitoneal chloral hydrate and subjected to SCI using the modified Allen weight-drop method in group H.The spinal cord was only exposed in group S.At 6,12,24 and 48 h after SCI(T1-4),6 rats in each group were randomly selected and sacrificed,and myocardial specimens were collected from the cardiac apex for microscopic examination of the cell morphology(with a transmission electron microscope) and for determination of cell apoptosis(by TUNEL assay),expression of Bax,Bcl-2 and VDAC2 protein and mRNA in cardiomyocytes(by Western blot and real-time polymerase chain reaction,respectively).The apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were calculated.Results Compared with group S,the apoptosis rate and ratios of Bax/Bcl-2 protein and mRNA were significantly increased at T1-4,the expression of VDAC2 protein and mRNA was significantly down-regulated at T2-4(P<0.05 or 0.01),and the pathologic changes of cardiomyocytes were aggravated in group H.Conclusion The mechanism of myocardial damage is related to down-regulation of mitochondrial VDAC2 expression in cardiomyocytes and promotion of cell apoptosis in rats with high-level SCI.
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Objective To explore the effects and mechanism of propofol on cognitive function of type 2 diabetic rats.Methods Ten of fifty adult male SD rats were fed with basic diet and allocated to control group.Another forty rats were fed with high sugar and high fat for 8 weeks and composite intraperitoneal injection of 1% streptozotocin (STZ)to establish model and then divided into four groups:diabetes group;low dose,middle dose and high dose of propofol group (diabetic rats were given intraperitoneal injection of 1% propofol 10,30,75 mg·kg-1·d-1 for 5 consecutive days).The cognitive functions were examined by Morris water maze from the first day after intraperitoneal injec-tion with propofol.The hippocampus were isolated for observing histopathologic alterations by HE staining and for the determinations of SOD,MDA,CAT,GSH and GSH-PX by colorimetry. Western blot was used to detect the expression of AGEs and RAGE.Results Compared to the control group,there was an obvious increased escape latent period,decreased the frequency of crossing platform,increased hippocampal neurons damage and MDA,decreased levels of SOD, CAT,GSH and GSH-PX,as well as the protein levels of AGEs and RAGE in diabetes group (P <0.05).There was no significant difference between diabetes group and low dose propofol of group on behavior ability and detection index.However,middle dose and high dose of propofol group showed more serious cognitive dysfunction,aggravated hippocampal neurons cells loss,increased oxidative stress as well as enhanced expression of AGEs and RAGE (P <0.05 ).Conclusion Multiple given sedative or anesthetic doses of propofol can aggravate the cognitive dysfunction and oxidative stress in type 2 diabetic rats,which may be related to increase the expression of AGEs and RAGE in brain tis-sue.
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Objective To evaluate the effect of diazocine on the inflammatory responses of the spi-nal cord in a rat model of incisional pain. Methods Seventy-two pathogen-free healthy adult male Sprague-Dawley rats, weighing 240-300 g, were divided into 3 groups(n=24 each)using a random number ta-ble: control group(group C), incisional pain group(group IP)and dezocine group(group D). A 10 mm longitudinal incision was made through skin, fascia and muscle of the plantar aspect of the right hind-paw in isoflurane-anesthetized rats. Dezocine 1 mg∕kg(diluted to 2 ml in 0.9% sodium chloride solution) was injected via the caudal vein at 15 min before skin incision in group D, and the equal volume of normal saline was injected via the caudal vein instead in group C. The mechanical paw withdrawal threshold (MWT)and thermal paw withdrawal latency(TWL)were measured at 12 h before skin incision(T0) and 2, 6 and 24 h after establishing the model(T1-3). The rats were sacrificed after measurement of the pain threshold at T3, and the spinal cord was removed for determination of the contents of interleukin-1beta (IL-1β), IL-6 and tumor necrosis factor-alpha(TNF-α)by enzyme-linked immunosorbent assay.Results Compared with group C, the MWT was significantly decreased and TWL was shortened at T1-3, and the contents of IL-1β, IL-6 and TNF-α were increased in IP and D groups(P<0.05). Compared with group IP, the MWT was significantly increased and TWL was prolonged at T1-3, and the contents of IL-1β, IL-6 and TNF-α were decreased in group D(P<0.05). Conclusion The mechanism by which dezocine re-duces incisional pain is partially related to inhibiting inflammatory responses of the spinal cord of rats.
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Objective To evaluate the effect of emulsified isoflurane postconditioning on mitophagy during myocardial ischemia-reperfusion (I/R) in rats.Methods Forty-eight pathogen-free healthy male Sprague-Dawley rats,aged 4-5 months,weighing 250-300 g,were divided into 4 groups (n=12 each) using a random number table:sham operation group (group S),group I/R,fat emulsion group (group F) and emulsified isoflurane postconditioning group (group EIP).Myocardial I/R was induced by occlusion of the anterior descending branch of the left coronary artery for 30 min followed by 120 min of reperfusion in pentobarbital sodium-anesthetized rats.Starting from 3 min before reperfusion,8％ emulsified isoflurane 2 ml/kg was intravenously infused over 8 min in group EIP,while 30％ fat emulsion 2 ml/kg was intravenously infused over 8 min in group F.Rats were sacrificed at the end of reperfusion,and hearts were removed for measurement of the myocardial infarct size (by 2,3,5-triphenyltetrazolium chloride staining),cell apoptosis (by TUNEL),mitochondrial membrane potential and expression of microtubule-associated protein 1 light chain 3 (LC3),Beclinl,P62,PINK1 and Parkin in cardiomyocytes (by using Western blot).Apoptosis index (AI) was calculated.Results Compared with group S,the myocardial infarct size and AI were significantly increased,the mitochondrial membrane potential was decreased,the expression of LC3,Beclinl,PINK1 and Parkin was up-regulated,and the expression of P62 was down-regulated in I/R,F and EIP groups (P＜0.05).Compared with group I/R,the myocardial infarct size and AI were significantly decreased,the mitochondrial membrane potential was increased,the expression of LC3,Beclinl,PINK1 and Parkin was down-regulated,and the expression of P62 was up-regulated in group EIP (P＜0.05).Compared with group F,the myocardial infarct size and AI were significantly decreased,the mitochondrial membrane potential was increased,the expression of LC3,Beclin1,PINK1 and Parkin was down-regulated,and the expression of P62 was up-regulated in group EIP (P＜0.05).Conclusion The mechanisin by which emulsified isoflurane postconditioning reduces myocardial I/R injury is related to inhibition of mitophagy in rats.
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Objective To evaluate the role of α7 nicotinic acetylcholine receptor (α7nAChR) in reduction of endotoxin-induced acute lung injury (ALI) by limb ischemic preconditioning in mice.Methods Eighty healthy male C57BL/6 mice,aged 8-10 weeks,weighing 22-26 g,were randomly divided into 5 groups (n =16 each) using a random number table:control group (group C),ALI group,limb ischemic preconditioning group (group P),α-bungarotoxin (α-BGT) group,and limb ischemic preconditioning +α-BGT group (group P+α-BGT).Normal saline 100 μl was intratracheally instilled in group C.In group ALI,lipopolysaccharide 5 mg/kg was intratracheally instilled (in normal saline) to establish the model of endotoxin-induced ALI.In group P,the mice were subjected to 6 cycles of 5-min ischemia of the right hindlimb followed by 5-min reperfusion,and then the model of ALI was established.In group α-BGT,α-BGT 1 μg/kg was injected intraperitoneally before establishment of the model.In group P+α-BGT,limb ischemic preconditioning was performed,α-BGT 1 μg/kg was then injected intraperitoneally,and the model of ALI was established.At 24 h after LPS instillation,6 mice were selected from each group and sacrificed,and lungs were removed for microscopic examination and for determination of wet and dry lung weight,myeloperoxidase (MPO) activities,contents of interleukin-lbeta (IL-1β),tumor necrosis factoralpha (TNF-α) and IL-6,and expression of α7nAChR and high mobility group box-1 (HMGB1) in lung tissues.The lung water content was calculated.The survival of the left 10 mice in each group was observed at 7 days after establishment of the model,and the survival rate was calculated.Results Compared with group C,the lung water content,MPO activities,contents of IL-1β,TNF-α and IL-6,and HMGB1 expression were significantly increased,α7nAChR expression was significantly down-regulated,and the 7-day survival rate was significantly decreased in group ALI(P＜0.05).Compared with group ALI,the lung water content,MPO activities,contents of IL-1β,TNF-α and IL-6,and HMGB1 expression were significantly decreased,α7nAChR expression was significantly up-regulated,and the 7-day survival rate was significantly increased in group P (P＜0.05).Compared with group P,the lung water content,MPO activities,contents of IL-1β,TNF-α and IL-6,and HMGB1 expression were significantly increased,α7nAChR expression was significantly down-regulated,and the 7-day survival rate was significantly decreased in group P+α-BGT (P＜0.05).Conclusion The mechanism by which limb ischemic preconditioning inhibits inflammatory responses and reduces endotoxin-induced ALI is related to activation of α7nAChR in mice.
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OBJECTIVE:To observe the influence and safety of dexmedetomidine (DEX) on intraoperative wake-up quality of patients underwent neurosurgical surgery. METHODS:126 patients with general anesthesia in neurosurgery were enrolled and randomized equally into observation group and control group,with 63 cases in each group. Control group was given target con-trolled infusion of propofol with plasma target concentration of 3-5 μg/ml and remifentanil with target effect site concentration of 2-6 ng/ml for anesthesia induction and maintenance,and then plasma target concentration of remifentanil decreased to 0.5 ng/ml 30 min before wake-up. Observation group received target controlled infusion of propofol with plasma target concentration of 3-5 μg/ml and remifentanil with target effect site concentration of 2-6 ng/ml for anesthesia induction and maintenance,and then given DEX 0.3 μg/kg intravenously 30 min before wake-up and maintained at 0.1 μg/(kg·h). MAP,HR,SBP,SaO2,serum levels of IgA,IgM,IgG,IL-6,IL-8 and TNF-α were observed in 2 groups 2 h before operation(T1)and after extubation(T2)as well as the occurrence of ADR during wake-up. RESULTS:There was no statistical significance in HR,MAP,SBP,SaO2,IgA,IgM, IgG,IL-6,IL-8 and TNF-α levels at T1 and SaO2 levels at T2 between 2 groups(P>0.05). HR,MAP,SBP,IL-6 and TNF-α lev-els of observation group decreased significantly at T2 and lower than those of control group;IgA,IgM and IgG increased signifi-cantly and higher than those of control group,with statistical significance (P0.05). CONCLUSIONS:DEX influence intraoperative wake-up quality of patients underwent neurosurgical surgery slightly,and can reduce inflammatory reaction with less ADR.
