Objective:To evaluate the role of leucine-rich repeat kinase 2 (LRRK2) in the spinal dorsal horn in diabetic neuropathic pain (DNP) and to determine whether the mechanism involved nuclear factor kappa B (NF-κB) signaling pathway in rats.Methods:SPF healthy male Sprague-Dawley rats, aged 8 weeks, weighing 205-238 g, were fed a high-sugar and high-fat diet and received intraperitoneal injection of streptozotocin to induce a type 2 diabetes mellitus model. Successful DNP model was defined as the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) being below 85% of the baseline in type 2 diabetes mellitus rats. Thirty-six rats with DNP were allocated into 3 groups ( n=12 each) using a random number table method: DNP group, MLi-2 (LRRK2 inhibitor) group, and MLi-2+ phorbol 12-myristate 13-acetate (PMA) (NF-κB activator) group. MLi-2 1 mg/kg was intrathecally injected at L 5-6 in MLi-2 group. In MLi-2+ PMA group, MLi-2 1 mg/kg was intrathecally injected, and 1 h later PMA 20 μg/10 μl was intrathecally injected. In group DNP, the equal volume of 5% dimethyl sulfoxide was intrathecally injected. Twelve healthy rats were randomly selected and served as control group (C group). The animals were fed a standard diet, normal saline 2 ml was intraperitoneally injected, and the equal volume of 5% dimethyl sulfoxide was intrathecally injected in group C. Intrathecal injection was performed once a day for 7 consecutive days. The MWT and TWL were measured at 1, 3, 5 and 7 days after intrathecal injection, and the motor nerve conduction velocity (MNCV) was measured using neuroelectrophysiological techniques. The L 4-6 segments of the spinal cord were collected, and histopathological changes were observed through HE staining. The co-localization of leucine-rich repeat kinase 2 (LRRK2) in the spinal dorsal horn with the microglial activation marker ionized calcium-binding adaptor molecule-1 (Iba-1) was observed by immunofluorescence staining. The L 4-6 segments of the spinal dorsal horn were harvested for determination of the level of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 (using enzyme-linked immunosorbent assay) and expression of LRRK2, Iba-1, nuclear factor kappa B (NF-κB) p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot). Results:Compared to C group, the TWL was significantly shortened, the MNCV was decreased, the percentage of cells co-expressing LRRK2 and Iba-1 in the spinal dorsal horn was increased, the contents of TNF-α, IL-1β and IL-6 were increased, the expression of LRRK2 and Iba-1 was up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was increased ( P<0.05), and histological examination revealed nuclear shrinkage and inflammatory cell infiltration in the spinal dorsal horn tissue in DNP group. Compared with DNP group, the MWT was significantly increased, the TWL was prolonged, the MNCV was elevated, the percentage of cells co-expressing LRRK2 and Iba-1 was decreased, the contents of TNF-α, IL-1β and IL-6 were decreased, the expression of LRRK2 and Iba-1 was down-regulated, the ratio of p-NF-κB p65/NF-κB p65 was decreased ( P<0.05), and pathological changes of the spinal dorsal horn tissue were significantly attenuated in MLi-2 group. Compared to MLi-2 group, the MWT was significantly decreased, the TWL was shortened, the MNCV was decreased, the percentage of cells co-expressing LRRK2 and Iba-1 was increased, the contents of TNF-α, IL-1β and IL-6 were increased, the expression of Iba-1 was up-regulated, and the ratio of p-NF-κB p65/NF-κB p65 was increased in MLi-2+ PMA group ( P<0.05). Conclusions:LRRK2 in spinal dorsal horn may be involved in the maintenance of DNP by promoting the inflammatory response mediated by microglial activation, and the mechanism may be related to the activation of NF-κB signaling pathway in rats.

Objective To explore the role and mechanism of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) in remifentanil (REM) resistance to hepatic ischemia-reperfusion injury (HIRI). Methods Forty SD rats were randomly divided into sham surgery group, HIRI group, HIRI+REM group, HIRI+PGC-1α inhibitor SR-18292 (HIRI+SR-18292) group and HIRI+REM+SR-18292 group, 8 rats in each group. HIRI rat models were constructed using non-invasive arterial clip occlusion method, and REM or SR-18292 were intravenously injected before surgery. The liver function indicators and liver tissue adenosine triphosphate (ATP) levels in the serum of rats were detected by assay kits. The activity levels of mitochondrial respiratory chain complexes Ⅲ and Ⅳ (COX-Ⅲ, COX-Ⅳ) in rat liver tissue were assessed by colorimetric methods. The pathological changes in rat liver tissue were observed by hematoxylin-eosin staining. Reactive oxygen species (ROS) and oxidative stress-related indicators in rat liver tissue were measured using the fluorescent probe (DCFH-DA) method and colorimetric methods. The mitochondrial DNA (mtDNA) copies and the expression levels of PGC-1α, nuclear respiratory factor-1 (NRF-1) and mitochondrial transcription factor A (TFAM) messenger RNA (mRNA) in rat liver tissue were quantified by real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). And the protein expression levels of PGC-1α, NRF-1 and TFAM in rat liver tissue were assessed by Western blotting. Results Compared with the sham group, rats in the HIRI group showed increased pathological scores and hepatic cell necrosis in liver tissue, elevated levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, and increased levels of ROS and malondialdehyde (MDA) in liver tissue. Additionally, there was a decrease in ATP content and the activity levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), COX-Ⅲ and COX-Ⅳ in liver tissue, as well as a decrease in mtDNA copies and the expression levels of PGC-1α, NRF-1 and TFAM mRNA and protein (all P<0.05). Compared with the HIRI group, rats in the HIRI+REM group exhibited decreased pathological scores and hepatic cell necrosis, reduced levels of serum ALT and AST, and decreased levels of ROS and MDA in liver tissue. There was also an increase in ATP content and the activity levels of SOD, GSH-Px, COX-Ⅲ and COX-Ⅳ in liver tissue, as well as an increase in mtDNA copies and the expression levels of PGC-1α, NRF-1 and TFAM mRNA and protein (all P<0.05). In contrast, rats in the HIRI+SR-18292 group showed increased pathological scores and hepatic cell necrosis, elevated levels of serum ALT and AST, and increased levels of ROS and MDA in liver tissue. There was a decrease in ATP content and the activity levels of SOD, GSH-Px, COX-Ⅲ and COX-Ⅳ in liver tissue, as well as a decrease in mtDNA copies and the expression levels of PGC-1α, NRF-1 and TFAM mRNA and protein (all P<0.05). Compared with the HIRI+REM group, rats in the HIRI+REM+SR-18292 group had increased pathological scores and hepatic cell necrosis, elevated levels of serum ALT and AST, and increased levels of ROS and MDA in liver tissue. There was a decrease in ATP content and the activity levels of SOD, GSH-Px, COX-Ⅲ and COX-Ⅳ in liver tissue, as well as a decrease in mtDNA copies and the expression levels of PGC-1α, NRF-1 and TFAM mRNA and protein (all P<0.05). Conclusions PGC-1α plays a role in regulating the process of REM resistance to HIRI by promoting mitochondrial biogenesis and reducing the levels of oxidative stress.

BACKGROUND:Cyclooxygenase-2 can significantly enhance depressive-like behavior in rats,and cyclooxygenase-2 inhibitors have antidepressant effects.Exercise can significantly reduce depressive-like behaviors in depressed patients.However,it is currently unclear whether exercise exerts an antidepressant effect by inhibiting cyclooxygenase-2.OBJECTIVE:To reveal the effects of exercise on cyclooxygenase-2 expression,microglia and astrocyte activation,oxidative stress and neuronal apoptosis in depressed rats,as well as the possible molecular mechanisms.METHODS:The rat model of depression was induced by chronic unpredictable mild stimulation.After modeling,the chronic unpredictable mild stimulation rats were randomly divided into stimulation group and wheel running group,with 10 rats in each group.In addition,10 normal rats were selected as the control group.The rats in the control group and stimulation group did not exercise.The rats in the wheel running group performed forced wheel running for a total of 4 weeks.Depressive-like behavior was evaluated by sucrose preference test.Hippocampal cyclooxygenase-2 expression was detected by immunofluorescence staining.The expression of cyclooxygenase-2,Iba-1,CD11b,CD45,glial fibrillary acid protein,Bcl-2,Bax,and cleaved caspase-3 proteins in the hippocampus was detected by western blot analysis.The cyclooxygenase-2 mRNA level in the hippocampus was detected by RT-PCR.The activities of antioxidant enzymes in hippocampal tissue homogenates were determined using kits.RESULTS AND CONCLUSION:Compared with stimulation group,sucrose consumption was increased;cyclooxygenase-2 expression in hippocampus was decreased;superoxide dismutase,catalase,and glutathione peroxidase levels in hippocampus were increased;malonaldehyde level was decreased;Iba1,CD11b,and CD45 protein expression levels in hippocampus were decreased,and glial fibrillary acid protein level in hippocampus was decreased.Bcl-2 protein expression levels in the hippocampus were increased,while Bax and cleaved caspase-3 levels were decreased in wheel running group(P＜0.05).This study showed that wheel running could reduce depressive-like behavior by inhibiting the expression of cyclooxygenase-2 in the hippocampus of chronic unpredictable mild stimulation rats.In addition,wheel running can exert antidepressant effects by inhibiting microglia and astrocyte activation,oxidative stress,and neuronal apoptosis in the hippocampus.

Objective:To evaluate the role of leucine-rich repeat kinase 2 (LRRK2) in the spinal dorsal horn in diabetic neuropathic pain (DNP) and to determine whether the mechanism involved nuclear factor kappa B (NF-κB) signaling pathway in rats.Methods:SPF healthy male Sprague-Dawley rats, aged 8 weeks, weighing 205-238 g, were fed a high-sugar and high-fat diet and received intraperitoneal injection of streptozotocin to induce a type 2 diabetes mellitus model. Successful DNP model was defined as the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) being below 85% of the baseline in type 2 diabetes mellitus rats. Thirty-six rats with DNP were allocated into 3 groups ( n=12 each) using a random number table method: DNP group, MLi-2 (LRRK2 inhibitor) group, and MLi-2+ phorbol 12-myristate 13-acetate (PMA) (NF-κB activator) group. MLi-2 1 mg/kg was intrathecally injected at L 5-6 in MLi-2 group. In MLi-2+ PMA group, MLi-2 1 mg/kg was intrathecally injected, and 1 h later PMA 20 μg/10 μl was intrathecally injected. In group DNP, the equal volume of 5% dimethyl sulfoxide was intrathecally injected. Twelve healthy rats were randomly selected and served as control group (C group). The animals were fed a standard diet, normal saline 2 ml was intraperitoneally injected, and the equal volume of 5% dimethyl sulfoxide was intrathecally injected in group C. Intrathecal injection was performed once a day for 7 consecutive days. The MWT and TWL were measured at 1, 3, 5 and 7 days after intrathecal injection, and the motor nerve conduction velocity (MNCV) was measured using neuroelectrophysiological techniques. The L 4-6 segments of the spinal cord were collected, and histopathological changes were observed through HE staining. The co-localization of leucine-rich repeat kinase 2 (LRRK2) in the spinal dorsal horn with the microglial activation marker ionized calcium-binding adaptor molecule-1 (Iba-1) was observed by immunofluorescence staining. The L 4-6 segments of the spinal dorsal horn were harvested for determination of the level of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 (using enzyme-linked immunosorbent assay) and expression of LRRK2, Iba-1, nuclear factor kappa B (NF-κB) p65 and phosphorylated NF-κB p65 (p-NF-κB p65) (by Western blot). Results:Compared to C group, the TWL was significantly shortened, the MNCV was decreased, the percentage of cells co-expressing LRRK2 and Iba-1 in the spinal dorsal horn was increased, the contents of TNF-α, IL-1β and IL-6 were increased, the expression of LRRK2 and Iba-1 was up-regulated, the ratio of p-NF-κB p65/NF-κB p65 was increased ( P<0.05), and histological examination revealed nuclear shrinkage and inflammatory cell infiltration in the spinal dorsal horn tissue in DNP group. Compared with DNP group, the MWT was significantly increased, the TWL was prolonged, the MNCV was elevated, the percentage of cells co-expressing LRRK2 and Iba-1 was decreased, the contents of TNF-α, IL-1β and IL-6 were decreased, the expression of LRRK2 and Iba-1 was down-regulated, the ratio of p-NF-κB p65/NF-κB p65 was decreased ( P<0.05), and pathological changes of the spinal dorsal horn tissue were significantly attenuated in MLi-2 group. Compared to MLi-2 group, the MWT was significantly decreased, the TWL was shortened, the MNCV was decreased, the percentage of cells co-expressing LRRK2 and Iba-1 was increased, the contents of TNF-α, IL-1β and IL-6 were increased, the expression of Iba-1 was up-regulated, and the ratio of p-NF-κB p65/NF-κB p65 was increased in MLi-2+ PMA group ( P<0.05). Conclusions:LRRK2 in spinal dorsal horn may be involved in the maintenance of DNP by promoting the inflammatory response mediated by microglial activation, and the mechanism may be related to the activation of NF-κB signaling pathway in rats.

BACKGROUND:Cyclooxygenase-2 can significantly enhance depressive-like behavior in rats,and cyclooxygenase-2 inhibitors have antidepressant effects.Exercise can significantly reduce depressive-like behaviors in depressed patients.However,it is currently unclear whether exercise exerts an antidepressant effect by inhibiting cyclooxygenase-2.OBJECTIVE:To reveal the effects of exercise on cyclooxygenase-2 expression,microglia and astrocyte activation,oxidative stress and neuronal apoptosis in depressed rats,as well as the possible molecular mechanisms.METHODS:The rat model of depression was induced by chronic unpredictable mild stimulation.After modeling,the chronic unpredictable mild stimulation rats were randomly divided into stimulation group and wheel running group,with 10 rats in each group.In addition,10 normal rats were selected as the control group.The rats in the control group and stimulation group did not exercise.The rats in the wheel running group performed forced wheel running for a total of 4 weeks.Depressive-like behavior was evaluated by sucrose preference test.Hippocampal cyclooxygenase-2 expression was detected by immunofluorescence staining.The expression of cyclooxygenase-2,Iba-1,CD11b,CD45,glial fibrillary acid protein,Bcl-2,Bax,and cleaved caspase-3 proteins in the hippocampus was detected by western blot analysis.The cyclooxygenase-2 mRNA level in the hippocampus was detected by RT-PCR.The activities of antioxidant enzymes in hippocampal tissue homogenates were determined using kits.RESULTS AND CONCLUSION:Compared with stimulation group,sucrose consumption was increased;cyclooxygenase-2 expression in hippocampus was decreased;superoxide dismutase,catalase,and glutathione peroxidase levels in hippocampus were increased;malonaldehyde level was decreased;Iba1,CD11b,and CD45 protein expression levels in hippocampus were decreased,and glial fibrillary acid protein level in hippocampus was decreased.Bcl-2 protein expression levels in the hippocampus were increased,while Bax and cleaved caspase-3 levels were decreased in wheel running group(P＜0.05).This study showed that wheel running could reduce depressive-like behavior by inhibiting the expression of cyclooxygenase-2 in the hippocampus of chronic unpredictable mild stimulation rats.In addition,wheel running can exert antidepressant effects by inhibiting microglia and astrocyte activation,oxidative stress,and neuronal apoptosis in the hippocampus.

Objective To study the effect of leucine rich repeat kinase 2(LRRK2)on pain sensitivity in neuro-pathic pain(NP)rats and explore its possible mechanism.Methods 48 SD rats were randomly divided into four groups:sham surgery(Sham),model,LRRK2 inhibitor(MLi-2),and LRRK2 inhibitor+p3 8 mitogen activated pro-tein kinase(MAPK)agonist(MLi-2+Anisomycin),with 12 rats in each group.The NP rat model was induced by chronic constriction injury(CCI)of the sciatic nerve.Intrathecal injection of MLi-2(1 mg/kg,10 μl)or Anisomy-cin(20 μmol/L,10 μl)was started from the 8th day after surgery,once a day for 7 consecutive days.Pain sensi-tivity tests were conducted before surgery(day 0)and on postoperative days 7 and 14,respectively.The changes in mechanical withdrawal threshold(MWT)and paw withdraw thermal latency(PWTL)were analyzed in each group of rats.ELISA was used to detect the levels of interleukin-1 β(IL-1β),IL-6 and tumor necrosis factor-α(TNF-α)in the dorsal horn of the rat spinal cord.Nissl staining was used to observe the pathological changes of neurons in rat spinal cord tissue.Immunofluorescence staining was used to observe the expression levels of ionized calcium-binding adapter molecule-1(Iba-1),a marker of microglia in the spinal cord of rats.Western blot was used to detect the protein expression levels of LRRK2,p-p38 mitogen activated protein kinase(MAPK),p38 MAPK,and Iba-1 in the dorsal horn of the rat spinal cord.Results Compared with the sham group,the model group showed a significant decrease in MWT and PWTL in the right hind limb of rats(P＜0.01).The levels of IL-1,IL-6,and TNF in the spi-nal dorsal horn tissue,as well as the expression levels of LRRK2,Iba-1 proteins and p-p38 MAPK/p38 MAPK pro-tein ratio significantly increased(P＜0.01).The proportion of Iba-1 positive cells in the spinal cord tissue signifi-cantly increased(P＜0.01),while Nissl bodies were significantly reduced(P＜0.01).Compared with the model group,the MLi-2 group showed a significant increase in MWT and PWTL in the right hind limb of rats(P＜0.01),a significant increase in Nissl bodies(P＜0.01),a significant decrease in the proportion of Iba-1 positive cells in the spinal cord tissue(P＜0.01),and a significant decrease in the levels of IL-1,IL-6,and TNF and the expression levels of LRRK2,Iba-1 proteins and p-p38 MAPK/p38 MAPK protein ratio(P＜0.01).However,Anisomychin in-tervention could activate the p38 MAPK signaling pathway and partially reverse the beneficial effects of MLi-2 on pain sensitivity and neuroinflammation in rats with neuropathic pain.Conclusion Inhibiting the expression of LRRK2 can alleviate pain sensitivity in NP rats induced by microglia activation mediated neuroinflammation,and its mechanism of action may be related to regulating the p38 MAPK signaling pathway.

Objective To investigate the role and mechanism of silent information regulator 1(SIRT1)-NOD-like receptor protein 3(NLRP3)axis in the effect of remifentanil against ischemia-reperfusion injury(IRI)in rat livers.SD rats were randomly divided into sham operation group(sham group),IRI group,IRI+remifentanil pretreatment group(IRI+RPC group),IRI+SIRT1 inhibitor EX-527 group(IRI+EX-527 group)and IRI+RPC+EX-527 group,with 8 rats in each group.The levels of serum alanine aminotransferase(ALT),aspartate aminotransferase(AST),lactate dehydrogenase(LDH),interleukin(IL)-1β and IL-18 of rats in each group were detected.The liver tissue pathology was observed.The apoptosis rate of hepatocytes in rats was detected.The expressions of SIRT1,NLRP3,cleaved cysteinyl aspartate specific proteinase-1(Cleaved Caspase-1)and Gasdermin D(GSDMD)proteins in rat liver tissue were detected.Results Compared with the sham group,the liver tissue pathological score and hepatocyte apoptosis rate of rats in the IRI group were increased,the serum ALT,AST,LDH,IL-1β,and IL-18 levels were increased,the relative expression of SIRT1 protein in liver tissue was decreased,and the relative expression of NLRP3,Cleaved Caspase-1,and GSDMD proteins were increased(all P<0.05).Compared with the IRI group,the liver tissue pathological score and hepatocyte apoptosis rate of rats in the IRI+RPC group were decreased,the serum ALT,AST,LDH,IL-1β,and IL-18 levels were decreased,the relative expression of SIRT1 protein in liver tissue was increased,and the relative expression of NLRP3,Cleaved Caspase-1,and GSDMD proteins were decreased;the liver tissue pathological score and hepatocyte apoptosis rate of rats in the IRI+EX-527 group were increased,the ALT,AST,LDH,IL-1β,and IL-18 levels were increased,the relative expression of SIRT1 protein in liver tissue was decreased,and the relative expression of NLRP3,Cleaved Caspase-1,and GSDMD proteins were increased(all P<0.05).Compared with the IRI+RPC group,the liver tissue pathological score and hepatocyte apoptosis rate in the IRI+RPC+EX-527 group were increased,the levels of ALT,AST,LDH,IL-1β,and IL-18 were increased,the relative expression of SIRT1 protein in liver tissue was decreased,and the relative expression of NLRP3,Cleaved Caspase-1,and GSDMD proteins were increased(all P<0.05).Conclusions SIRT1 may participate in the regulation of remifentanil against rat liver IRI by inhibiting NLRP3 mediated cell pyroptosis.

Objective:To evaluate the role of spinal Leucine-rich Repeat Kinase 2 (LRRK2) in neuropathic pain in rats.Methods:Fifty SPF healthy male Sprague-Dawley rats, aged 6-7 weeks, weighing 210-245 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (C group), neuropathic pain group (NP group), low dose GNE-7915 group (low-dose GNE-7915 group), medium-dose GNE-7915 group (medium-dose GNE-7915 group), and high-dose GNE-7915 group (high-dose GNE-7915 group). Neuropathic pain was induced by the spared nerve injury in anesthetized rats. At 7 days after developing the model, LRRK2 inhibitor GNE-7915 12.5, 25.0 and 50.0 mg/kg were intraperitoneally injected in low-, medium- and high-dose GNE-7915 groups, respectively. The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before developing the model, at 7 days after developing the model, and at 4 h after injecting the inhibitor. After measurement of the pain threshold, the rats were sacrificed and the spinal cord tissues were taken for determination of the positive expression of ionized calcium-binding adapter molecule 1(Iba-1) (by immunofluorescence staining), contents of interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1) and IL-18 (by enzyme-linked immunosorbent assay), positive expression of phosphorylated LRRK2 (p-LRRK2) (by immunofluorescence staining), and expression of LRRK2, IL-1β, MCP-1 and IL-18 (by immunoblotting). The ratio of p-LRRK2/LRRK2 was calculated. Results:Compared with C group, the MWT was significantly decreased, the TWL was shortened, the proportion of Iba-1 and p-LRRK2 positive cells in spinal cord tissues, contents of IL-1β, MCP-1 and IL-18, and p-LRRK2/LRRK2 ratio were increased, and the expression of IL-1β, MCP-1 and IL-18 proteins was up-regulated in NP group ( P<0.05). Compared with NP group, the MWT was significantly increased, the TWL was prolonged, the proportion of Iba-1 and p-LRRK2 positive cells in spinal cord tissues, contents of IL-1β, MCP-1 and IL-18, and p-LRRK2/LRRK2 ratio were decreased, and the expression of IL-1β, MCP-1 and IL-18 proteins was down-regulated in low-, medium- and high-dose GNE-7915 groups ( P<0.05). Conclusions:LRRK2 in the spinal cord may be involved in the pathophysiological mechanism of neuropathic pain by activating microglia and inducing inflammatory responses in rats.

Objective To evaluate the efficacy and safety of dezocine versus sufentanil for postoperative patient-controlled epidural analgesia (PCEA).Methods PubMed,EMBASE,Cochrane Library,ISI Web of knowledge,Chinese Biomedical Database,Chinese Science-Technology Journal Database,China Journal Full-text Database and Wanfang Database were searched for randomized controlled trials involving the efficacy and safety of dezocine and sufentanil for PCEA from the date of database establishment up to April 2014.Randomized controlled trials met the inclusion criteria were included,and the data were extracted.The quality of the trials was evaluated according to Cochrane Handbook 5.1.0 criteria.Meta-analysis was conducted using RevMan 5.1 software.Results Seven studies involving 760 patients were included in this meta-analysis.The results of meta-analyses showed that there was no significant difference between dezocine group and sufentanil group in VAS scores at 4,8,12,16,24 and 48 h after surgery and in Ramsay sedation scores at 4,12,24 and 48 h after surgery,and the incidence of adverse reactions (postoperative nausea and vomiting,pruritus,urinary retention and somnolence) was significantly lower in dezocine group than in sufentanil group,and there was no significant difference in the incidence of respiratory depression and dizziness between dezocine group and sufentanil group.Conclusion Dezocine provides better efficacy and safety for postoperative PCEA than sufentanil.