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Objective:To evaluate the role of ERBB2 interacting protein (Erbin)in liver tissues in blood coagulation of septic mice.Methods:Thirty SPF healthy male C57BL/6 mice and 30 Erbin knockout mice, aged 8-10 weeks, weighing 20-30 g, were divided into wild-type+ sham operation group (WT+ Sham group), wild-type+ sepsis group (WT+ SEP group), Erbin gene knockout+ sham operation group (EKO+ Sham group) and Erbin gene knockout+ sepsis group (EKO+ SEP group) by a random number table method, with 15 animals in each group. The mouse sepsis model was prepared by the cecal ligation and perforation method in anesthetized animals. Eye blood samples were collected at 24 h after surgery and liver tissues were obtained for microscopic examination of histopathological changes (by HE staining) which were scored and for determination of plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (by colorimetry), expression of Erbin and tissue factor (TF) (by Western blot), expression of tissue plasminogen activator (t-PA) and fibrinogen (Fib)mRNA (by quantitative polymerase chain reaction), concentrations of PT, APTT, thrombin time (TT) and Fib (by automatic coagulation analyzer), and plasma TF and interleukin-6 (IL-6) concentrations (by enzyme-linked immunosorbent assay).Results:Compared with WT+ Sham group, the lung injury score was significantly increased, the expression of TF, t-PA mRNA and FGA mRNA was up-regulated, PT, APTT and TT were prolonged, the plasma Fib concentration was increased, and the activities of ALT and AST and concentrations of TF and IL-6 in plasma were increased in WT+ SEP group ( P<0.05). Compared with WT+ SEP group, the lung injury score was significantly increased, the expression of TF, t-PA mRNA and FGA mRNA was up-regulated, PT, APTT and TT were prolonged, the plasma Fib concentration was increased, and the activities of ALT and AST and concentrations of TF and IL-6 in plasma were increased in EKO+ SEP group ( P<0.05). Conclusions:Erbin in liver tissues exerts an endogenous protective effect on blood coagulation by inhibiting the up-regulation of TF expression in septic mice.
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Objective:To investigate the mid-term clinical outcomes of arthroscopic vertical mattress suturing for shoulder recurrent anterior dislocation combined with joint laxity.Methods:A retrospective case series study was performed on the clinical data of 11 patients with recurrent anterior shoulder dislocation combined with joint laxity admitted to the First Affiliated Hospital, Army Medical University from January 2018 to September 2021. The patients included 10 males and 1 female, aged 18-38 years [(22.8±5.5)years]. All the patients received treatment with arthroscopic vertical mattress suturing. The Oxford shoulder instability score, Rowe shoulder instability score, and simple shoulder test (SST) score were compared before operation, at 6 months after operation and at the final follow-up. The degree of joint capsule laxity and length of capsular redundancy (evaluated by MRI) were compared before operation and at the final follow-up. The results of the supine apprehension test, re-dislocation and postoperative complications such as iatrogenic vascular and nerve injuries were observed at the final follow-up. Also, the correlation between the radiological changes in the joint capsule and the shoulder function was analyzed by Spearman correlation coefficient.Results:All the patients were followed up for 20-64 months [(40.7±18.6)months]. Before operation, at 6 months after surgery and at the final follow-up, the values of Oxford shoulder instability score were (41.2±4.7)points, (49.5±3.0)points and (57.6±3.0)points; the values of Rowe shoulder instability score were (28.6±9.5)points, (77.7±7.2)points and (94.1±10.9)points; and the values of SST score were (7.6±1.3)points, (9.8±1.0)points and (11.6±0.9)points, respectively. The Oxford shoulder instability score, Rowe shoulder instability score and SST at 6 months after operation and at the final follow-up were significantly better than those before operation, and those at the final follow-up were significantly better than those at 6 months after operation (all P<0.05). The MRI showed that the degree of joint capsular laxity and length of capsular redundancy were 1.5±0.2 and (19.7±2.5)mm before operation and were 1.3±0.2 and (12.9±3.7)mm at the final follow-up, respectively ( P<0.05 or 0.01). The supine apprehension test was negative at the final follow-up, with no re-dislocation or postoperative complications such as iatrogenic vascular or nerve injuries. Correlation analysis showed a negative correlation between the degree of joint capsular laxity and the Oxford shoulder instability score ( r=-0.62, P<0.05) and that of the length of capsular redundancy with the Oxford shoulder instability score ( r=-0.80, P<0.01), the Rowe shoulder stability score ( r=-0.73, P<0.01) and the SST score ( r=-0.75, P<0.01). Conclusions:Arthroscopic vertical mattress suturing has good mid-term clinical outcome for recurrent shoulder anterior dislocation combined with joint laxity, improving the shoulder function and reducing complications, wihch is associated with decreased joint capsule laxity and length of capsular redundancy.
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@#Objective To explore the relationship between preoperative fasting plasma glucose (FPG) and postoperative pulmonary complications (PPCs) in type 2 diabetic patients undergoing elective thoracoscopic lung resection, and provide a reference for prediction and prevention of PPCs in the clinic. Methods A retrospective analysis was performed on the type 2 diabetic patients who underwent elective thoracoscopic lung resection for the first time in our hospital from January 2017 to March 2021. According to the level of FPG one day before the operation, the patients were divided into three groups: a hypoglycemia group (<6.1 mmol/L), a medium level blood glucose group (≥6.1 mmol/L and <8.0 mmol/L) and a high blood glucose group (≥8.0 mmol/L). Besides, the patients were divided into a PPCs group and a non-PPCs group according to whether PPCs occurred. The risk factors for PPCs were analyzed by logistic regression analysis, and the predictive value of preoperative FPG level on PPCs was estimated by the area under the receiver operating characteristic curve (AUC). Results A total of 130 patients were included, including 75 (57.7%) males and 55 (42.3%) females with an average age of 63.5±9.0 years. Logistic regression analysis showed that compared to non-PPCs patients, the level of preoperative FPG (P=0.023) and smoking history ratio (P=0.036) were higher and the operation time was longer (P=0.004) in the PPCs patients. High FPG level on preoperative day 1 and longer operation time were associated with PPCs risk. Besides, the preoperative FPG of 6.79 mmol/L was the threshold value to predict the occurrence of PPCs [AUC=0.653, 95%CI (0.559, 0.747), P=0.003]. Conclusion There is a certain correlation between preoperative FPG level and postoperative PPCs, which may be used as an index to predict the occurrence of PPCs.
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Objective:To evaluate the relationship between Erbin and Bax/Bcl-xL-mediated cell apoptosis during sepsis-induced acute kidney injury in mice.Methods:Thirty-two SPF male wild type C57BL/6 mice, 32 SPF male Erbin (-/-) C57BL/6 mice, aged 6-8 weeks, weighing 20-30 g, were divided into 2 groups ( n=16 each) using the random number table method: wild type sham operation group (WT+ Sham group), wild type sepsis group (WT+ S group), Erbin(-/-) sham operation group (EKO+ Sham group), and Erbin(-/-) sepsis group (EKO+ S group). The sepsis model was established using the moderate cecal ligation and puncture (CLP) in anesthetized animals.The survival rates within 7 days after CLP were recorded.The serum concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), IL-1β, creatinine (Cr), blood urea nitrogen (BUN) and lactic dehydrogenase (LDH) were determined at 24 h after CLP.Then the renal tissues were taken for assessment of renal injury which was scored and for determination of the apoptosis rate (by TUNEL) and expression of cleaved-caspase-3, Bcl-xL and Bax (by Western blot). Results:Compared with sham operation groups, the survival rates were significantly decreased, the serum concentrations of IL-1β, IL-10, TNF-α, Cr, BUN and LDH, renal injury score and apoptosis rate were increased, the expression of Bax and cleaved-caspase-3 was up-regulated, and the expression of Bcl-xL was down-regulated in sepsis groups ( P<0.05). Compared with WT+ S group, the survival rates were significantly decreased, the serum concentrations of IL-1β, LDH, TNF-α, Cr and BUN and renal injury score were increased, the serum concentration of IL-10 was decreased, the apoptosis rate of renal tissues was increased, the expression of Bax and cleaved-caspase-3 was up-regulated, and the expression of Bcl-xL was down-regulated in EKO+ S group ( P<0.05). Conclusions:Erbin can inhibit Bax/Bcl-xL-mediated cell apoptosis and is involved in endogenous protective mechanism against sepsis-induced acute kidney injury in mice.
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Objective:To evaluate the role of ErbB2 interacting protein (Erbin) in sepsis-associated encephalopathy (SAE) in mice and the relationship with nod-like receptor thermoprotein domain associated protein 3 (NLRP3) inflammasomes.Methods:Sixty SPF-grade healthy male wild-type C57BL/6 mice and 60 Erbin (-/-)C57BL/6 mice, aged 8-10 weeks, weighing 20-25 g, were divided into 4 groups ( n=30 each) by a random number table method: wild-type sham operation group (WT+ Sham group), wild-type SAE group (WT+ SAE group), Erbin (-/-) sham operation group (EKO+ Sham group) and Erbin (-/-) plus SAE group (EKO+ SAE group). The model of SAE was established by cecal ligation and perforation in anesthetized mice.Open field test (total distance moved) was performed at 7 days after establishing the model, new object recognition test (recognition index) was performed at 8 days after establishing the model, and Morris water maze test (time of staying at target quadrant) was performed at 10 days after establishing the model.The mice were sacrificed, and hippocampal tissues were removed for microscopic examination of pathologic changes (by HE staining) and for determination of neuron count, expression of NLRP3, caspase-1 and apoptosis-associated speck-like protein containing a CARD (ASC) (by Western blot), the number of NLRP3 positive cells (by immunohistochemistry), and contents of interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α) and IL-18 (by enzyme-linked immunosorbent assay). The cell survival rate was calculated. Results:Compared with group WT+ Sham, the time of staying at target quadrant was significantly shortened, the recognition index and cell survival rate were decreased, the contents of IL-1β, IL-18 and TNF-α and the number of NLRP3 positive cells were increased, and the expression of NLRP3, caspase-1 and ASC was up-regulated in group WT+ SAE ( P<0.05). Compared with group EKO+ Sham, the time of staying at target quadrant was significantly shortened, the recognition index and cell survival rate were decreased, the contents of IL-1β, IL-18 and TNF-α and the number of NLRP3 positive cells were increased, and the expression of NLRP3, caspase-1 and ASC was up-regulated in group EKO+ SAE ( P<0.05). Compared with group WT+ SAE, the time of staying at target quadrant was significantly shortened, the recognition index and cell survival rate were decreased, the contents of IL-1β, IL-18 and TNF-α and the number of NLRP3 positive cells were increased, and the expression of NLRP3, caspase-1 and ASC was up-regulated in group EKO+ SAE ( P<0.05). There was no significant difference in total distance moved between the four groups ( P>0.05). Conclusion:Erbin can exert endogenous protection by inhibiting the activation of NLRP3 inflammasomes in mice with SAE.
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Objective To evaluate the role of phosphatidylinositol 3-kinase ( PI3K)∕protein kinase B ( Akt) signaling pathway in propofol-induced reduction of intestinal ischemia-reperfusion ( I∕R) injury in rats. Methods Thirty-two healthy male Sprague-Dawley rats, aged 2-3 months, weighing 225-275 g, were divided into 4 groups ( n=8 each) using a random number table method: sham operation group ( Sham group), intestinal I∕R group ( I∕R group), propofol group ( P group), and PI3K inhibitor wortmannin plus propofol group ( W+P group) . Intestinal ischemia was induced by occluding the superior mesenteric ar-tery for 45 min followed by 2 h of reperfusion to establish the model of intestinal I∕R injury. Propofol was in-travenously infused at a rate of 20 mg·kg-1 ·h-1 starting from the onset of reperfusion until the end of reper-fusion in group P. Wortmannin 15 μg∕kg was intravenously injected at 25 min before reperfusion, and propofol was intravenously infused at a rate of 20 mg·kg-1 ·h-1 starting from the onset of reperfusion until the end of reperfusion in group W+P. Rats were sacrificed at 2 h of reperfusion, and small intestinal tissues were obtained for microscopic examination of pathologic changes of intestinal mucosa and for determination of wet∕dry weight ratio (W∕D ratio), malondialdehyde (MDA) content (by thiobarbituric acid colorimetric method) , superoxide dismutase ( SOD ) activity ( using xanthine oxidase method ) , myeloperoxidase ( MPO) activity ( by MPO assay) , and phosphorylated Akt ( p-Akt) expression ( by Western blot) . Intes-tinal damage was assessed and scored according to Chiu. Results Compared with group Sham, Chiu' s score, W∕D ratio, MDA content and MPO activity were significantly increased, the SOD activity was de-creased, and p-Akt expression was down-regulated in group I∕R (P<0. 05). Compared with group I∕R, Chiu's score, W∕D ratio, MDA content and MPO activity were significantly decreased, the SOD activity was increased, and p-Akt expression was up-regulated in group P (P<0. 05). Compared with group P, Chiu's score, W∕D ratio, MDA content and MPO activity were significantly increased, the SOD activity was decreased, and p-Akt expression was down-regulated in group W+P (P<0. 05). Conclusion The mechanism by which propofol reduces intestrnal I∕R injury is related to activating PI3K∕Akt signaling path-way and inhibiting inflammatory and oxidative stress responses in rats.
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Objective To evaluate the effect of anti-myosin monoclonal antibodies-nuclear factor kappa B (NF-κB) decoy oligodeoxynucleotides-lipofectamine compound (mAb2G4-ODN-lip) on myocardial ischemia-reperfusion (I/R) injury in rats.Methods Forty clean-grade healthy adult male Sprague-Dawley rats,aged 8-10 weeks,weighing 240-260 g,were divided into 4 groups (n=10 each) using a random number table:sham operation group (group S),myocardial I/R group (group I/R),ODN-lip group (group ODN) and mAb2G4-ODN-lip group (group mAb2G4).Myocardial I/R was induced by occlusion of the left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion.In ODN and mAb2G4 groups,ODN-lip (100 μg ODN) and mAb2G4-ODN-lip (100 μg ODN) compounds were injected via the femoral vein,respectively,immediately after onset of ischemia.The left anterior descending branch of coronary artery was only occluded but not ligated in group S.The animals were sacrificed at 120 min of reperfusion and myocardial specimens of the left ventricle on the ischemic side were obtained for examination of the pathological changes (using haematoxylin and eosin staining) and for determination of the expression of NF-κB (by Western blot) and contents of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) (by enzyme-linked immunosorbent assay).Results Compared with group S,the expression of NF-κB was significantly up-regulated,and the contents of TNF-α and IL-6 were increased in I/R,ODN and mAb2G4 groups (P< 0.05).Compared with group I/R,the expression of NF-κB was significantly down-regulated,and the contents of TNF-α and IL-6 were decreased in ODN and mAb2G4 groups (P<0.05).Compared with group ODN,the expression of NF-κB was significantly down-regulated,and the contents of TNF-α and IL-6 were decreased in group mAb2G4 (P<0.05).The pathological changes of myocardial tissues were significantly attenuated in group I/R,group ODN and group mAb2G4 in turn.Conclusion mAb2G4-ODN-lip can mitigate myocardial I/R injury in rats.
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Objective To evaluate the effect of oxycodone preconditioning on mitochondrion-dependent apoptosis in liver ceils during intestinal ischemia-reperfusion (I/R) in rats.Methods Fifty-four healthy male Sprague-Dawley rats,weighing 200-300 g,were divided into 9 groups (n=6 each) using a random number table:sham operation group (group S),I/R group,oxycodone preconditioning group (group OP),μ receptor blocker CTOP group (group CTOP),δ receptor blocker naltrindole (NTD) group (group NTD),κ receptor blocker nor-binaltorphimne (BNI) group (group BNI),CTOP plus oxycodone preconditioning group (group CTOP+OP),NTD plus oxycodone preconditioning group (group NTD+ OP),and BN1 plus oxycodone preconditioning group (group BNI+OP).The model of intestinal I/R was established by occluding the superior mesenteric artery for 45 min followed by 2 h reperfusion.Oxycodone 0.5 mg/kg was injected intravenously at 10 min prior to ischemia in OP,COTP+OP,NTD+OP and BNI+ OP groups.COTP 1 mg/kg and NTD 5 mg/kg were injected intravenously at 20 min prior to ischemia in COTP+OP and NTD+OP groups,respectively.BNI 5 mg/kg was injected intravenously at 25 min prior to ischemia in group BNI+OP.CTOP 1 mg/kg and NTD 5 mg/kg were injected intravenously at 10 min prior to ischemia in CTOP and NTD groups,respectively.BNI 5 mg/kg was injected intravenously at 15 min prior to ischemia in group BNI.The superior mesenteric artery was only exposed but not occluded in group S.The rats were sacrificed at 2 h of reperfusion,and livers were removed for determination of apoptosis in liver cells (using TUNEL) and expression of Bcl-2 and caspase-3 in liver tissues (by immunohistochemistry).The apoptosis index (AI) was calculated.Results Compared with group S,AI was significantly increased,the expression of Bcl-2 was down-regulated and the expression of caspase-3 was up-regulated in the other eight groups (P<0.05).Compared with group I/R,AI was significantly decreased,the expression of Bcl-2 was up-regulated,and the expression of caspase-3 was down-regulated in group OP (P<0.05).Compared with group OP,AI was significantly increased,Bcl-2 expression was down-regulated,and caspase-3 expression was up-regulated in COTP+OP,NTD+OP and BNI+OP groups (P<0.05).Conclusion The mechanism by which oxycodone preconditioning activates μ,δ and κ receptors and reduces intestinal I/R injury may be related to inhibiting mitochondrion-dependent apoptosis in rats.
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Objective To evaluate the influence of preconditioning with and anti-myosinmonoclonal antibody (mAb2G4)-nuclear factor-kappa B decoy oligodeoxynucleotide (ODN)-lipofectamine (lip) on hypoxia-reoxygenation (H/R) injury in H9c2 cardiomyocytes.Methods H9c2 cardiomyocytes were seeded in 6-well plate at the density of 1×105/ml (2 ml/well),and were divided into 3 groups (n=9 each) using a random number table:control group (group C),H/R group and mAb2G4-ODN-lip group (group MOL).The cells underwent 2 h of hypoxia in an air-tight bag,followed by 1 h reoxygenation.In MOL group,the cells were treated with mAb2G4-ODN-lip (2 μg ODN) for 4 h and then cultured in the common culture medium for 8 h before hypoxia.At the end of reoxygenation,proliferation of cells was measured using MTT assay,and the cells and supernatant of the culture medium were collected to determine the activity of lactate dehydrogenas (LDH),content of malondialdehyde (MDA),concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) (by ELISA).The rate of proliferation inhibition was calculated.Results Compared with group C,the rate of proliferation inhibition,LDH activity,MDA content,and concentrations of TNF-α and IL-6 were significantly increased in the other two groups.Compared with group H/R,the rate of proliferation inhibition,LDH activity,MDA content,and concentrations of TNF-α and IL-6 were significantly decreased in MOL group.Conclusion mAb2G4-ODN-lip can mitigate H/R injury in H9c2 cardiomyocytes.
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Objective To evaluate the effect of oxycodone preconditioning on liver injury induced by intestinal ischemia-reperfusion (I/R) in rats and the role of different opioid receptors.Methods Fiftyfour adult male Sprague-Dawley rats, weighing 200-300 g, were randomly divided into 9 groups (n =6 each) using a random number table: sham operation group (group S), group I/R, oxycodone preconditioning group (group OP) , μ receptor antagonist CTOP group (group CTOP) , δ receptor antagonist naltrindole group (group NTD), κ receptor antagonist nor-binaltorphimne group (group BNI), CTOP + oxycodo ne preconditioning group (group CTOP+OP) , naltrindole + oxycodone preconditioning group (group NTD+ OP) , and nor-binaltorphimne + oxycodone preconditioning group (BNI+OP).The model of intestinal I/R was established by occlusion of the superior mesenteric artery for 45 min followed by 2 h reperfusion in anesthetized rats.The superior mesenteric artery was only exposed, but not occluded in group S.In OP,COTP+OP, NTD+OP and BNI+OP groups, oxycodone 0.5 mg/kg was injected intravenously at 10 min prior to ischemia.COTP 1 mg/kg and naltrindole 5 mg/kg were injected intravenously at 20 min prior to ischemia in COTP+OP and NTD+OP groups, respectively.Nor-binaltorphimne 5 mg/kg was injected intravenously at 25 min prior to ischemia in group BNI+OP.In CTOP and NTD groups, the corresponding doses of CTOP and naltrindole were injected intravenously at 10 min prior to ischemia.In group BNI, the corresponding dose of nor-binaltorphimne was injected intravenously at 15 min prior to ischemia.The rats were sacrificed at 2 h of reperfusion, and left hepatic lobes were removed for microscopic examination and for detection of apoptosis in liver cells (using TUNEL).The apoptosis index (AI) was calculated.Results Compared with group S, the AI was significantly increased in the other groups (P<0.05).Compared with group I/R, the AI was significantly decreased (P<0.05) , and the pathological changes of livers were reduced in OP, COTP+OP, NTD+OP and BNI+OP groups, and no significant change was found in AI and pathological changes of livers in CTOP, NTD and BNI groups (P>0.05).Compared with group OP, the AI was significantly increased (P<0.05), and the pathological changes of livers were aggravated in COTP+ OP, NTD+OP and BNI+OP groups.There was no significant difference in AI and pathological changes of livers among groups COTP+OP, NTD+OP and BNI+OP (P>0.05).Conclusion Oxycodone preconditioning can mitigate liver injury induced by intestinal I/R in rats, and μ, δ and κ receptors mediate the role with comparable effects.
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Objective To evaluate the effects of different doses of oxycodone on renal ischemiareperfusion (I/R) injury in rats.Methods Forty adult male Sprague-Dawley rats, weighing 220-300 g, aged 10-13 weeks, were randomly divided into 5 groups (n =8 each) using a random number table: sham operation group (group S), group I/R, and low, medium and high doses of oxycodone groups (OL, OM and OH groups).After the rats underwent right nephrectomy, the renal I/R was induced by occlusion of the left renal artery and vein for 45 min with atraumatic microclips followed by 3 h reperfusion in I/R, OL, OM and OH groups.In group S, right nephrectomy was performed, and the left renal artery, vein and ureter were isolated without occluding blood flow.In OL, OM and OH groups, oxycodoue 2, 4, and 6 mg/kg were infused intravenously, respectively, immediately after onset of ischemia.At 3 h of reperfusion, blood samples were taken from the abdominal aorta to determine the concentrations of serum blood urea nitrogen (BUN) and creatiniue (Cr) concentrations.After blood sampling, the animals were sacrificed, and the left kidneys were removed for determination of tumor necrosis factor-alpha (TNF-α) , interleukin-6 (IL-6) and IL-8 and IL-10 contents (by using enzyme-linked immunosorbent assay), and malondialdehyde (MDA) content (by thiobarbituric acid method), and superoxide dismutase (SOD) activity (using xanthine oxidase method).Results Compared with group S, the serum BUN and Cr concentrations, and contents of TNF-α, IL-6, IL-8 and MDA in renal tissues were significantly increased, and the IL-10 content and SOD activity in renal tissues were decreased in the other four groups (P<0.05).Compared with group I/R, the serum BUN and Cr concentrations, and contents of TNF-α, IL-6, IL-8 and MDA in renal tissues were significantly decreased, and the IL-10 content and SOD activity in renal tissues were increased in OL, OM and OH groups (P<0.05).The serum BUN and Cr concentrations, and contents of TNF-α,IL-6, IL-8 and MDA in renal tissues were gradually decreased, and the IL-10 content and SOD activity in renal tissues were gradually increased with increasing dosage of oxycodone in OL, OM and OH groups (P< 0.05).Conclusion Oxycodone 2, 4, and 6 mg/kg can alleviate renal I/R injury in a dose-dependent manner in rats, and the mechanism is related to inhibition of inflammatory responses and oxidative stress response.