Objective : To pathological changes and inducible nitric oxide synthase(iNOS), phosphorylated insulin receptor substrate 1 serine 307(p-IRS1ser 307), phosphorylated protein kinase B serine 473(p-AKTser 473), glycogen synthase kinase-3β(GSK-3β), and gluconeogenic synthase(GS) proteins were observed in the liver of rats under the condition of chronic intermittent hypoxia-replicated oxygen in control. And to explore the role of iNOS/IRS1/AKT/GSK-3β signaling pathway in chronic intermittent hypoxia-induced insulin resistance. Methods : Forty SD rats were randomly divided into a control group(NC group) and an experimental group(CIH group), with 20 rats in each group. The NC group was placed in a normoxic environment for 12 weeks, while the CIH group was first subjected to intermittent hypoxia for 8 weeks, and then resumed normoxic rearing until the 12th week. Fasting blood glucose(FBG) and fasting insulin(FINS) were measured at baseline, week 8 and week 12, and liver tissues were taken for pathology and measurement of iNOS, p-IRS1ser 307, p-AKTser 473, GSK3β and GS levels, to compare the differences between groups. Results: t baseline, there was no significant difference in liver pathology between the two groups, and the observed indexes were not statistically significant(P>0.05); at 8 weeks, compared with the NC group, liver pathology in the CIH group showed significant disorganization of hepatic blood sinusoids and hepatocyte cords, obvious hepatocyte edema, smaller nuclei, increased lymphocyte infiltration, and a small number of fat vacuoles, significantly higher levels of FBG, FINS, insulin resistance index(HOMA-IR), iNOS mRNA, p-IRS1ser 307 protein, GSK-3β protein levels, and decreased p-AKTser 473 protein and GS protein levels, all of which were statistically significant(allP<0.05). IRS1ser 307 protein, GSK-3β protein levels were increased, p-AKTser 473 protein and GS protein levels were decreased, and the differences were statistically significant(allP<0.05); at 12 weeks, no lymphocyte infiltration was seen in the CIH group compared with that of the NC group and fat vacuoles significantly increased, and there was no improvement in the other pathological damage that had already occurred, and the levels of p-AKTser 473 protein significantly increased. AKTser 473 protein level significantly increased, p-IRS1ser 307 protein and GS protein levels were significantly reduced, all of which were statistically significant(allP<0.05), and the rest of the observational indexes were not statistically significant. Pearson′s correlation analysis showed that HOMA-IR of CIH group was significantly positively correlated with the levels of iNOS mRNA, p-IRS1ser 307 protein, and GSK-3β protein at 8 weeks(r=0.874, 0.817,0.872;allP<0.05), and significantly negatively correlated with the levels of p-AKTser 473 protein and GS protein(r=-0.886,-0.879;allP<0.05). Conclusion Chronic intermittent hypoxia can lead to hepatic pathological damage that cannot be reversed even by reoxygenation interventions and may mediate the development of insulin resistance by upregulating the IRS1/AKT/GSK-3β signaling pathway through the upregulation of iNOS mRNA expression.

Objective:To explore the effects of childhood trauma on resting blood pressure, heart rate, and heart rate variability in patients with depression.Methods:A cross-sectional study was designed to prospectively collect clinical data on a total of 163 patients with depression, including 47 males and 116 females, aged 18-50 years,with mean[ M( Q1, Q3)] [29.0, (21.0, 37.0)]years, who were either the outpatients or the inpatients in the Mental Health Center of the First Hospital of Hebei Medical University from September 2022 to June 2024. The Childhood Trauma Questionnaire-Short form (CTQ-SF) was used to assess the experience of abuse and neglect during childhood. According to the CTQ-SF score, the subjects were divided into a trauma group ( n=80) and a non-trauma group ( n=83). The 17-item Hamilton Depression Scale (HAMD 17) and Hamilton Anxiety Scale (HAMA) were used to assess depressive and anxiety symptoms in the participants, respectively. A digital blood pressure monitor and an autonomic nervous system response detector were employed to measure resting blood pressure, heart rate, and heart rate variability (HRV). Spearman correlation analysis was used to examine the relationships between childhood trauma and resting blood pressure, heart rate, and HRV. Multiple linear regression analysis was performed to analyze factors influencing these parameters. The Bootstrap method was employed to test the potential mediating role of parasympathetic nervous system activity in the relationships between childhood trauma and resting blood pressure, and heart rate. Results:No significant difference was observed in resting heart rate between the trauma and non-trauma groups ( P>0.05). However, the trauma group exhibited higher resting systolic and diastolic blood pressure [(123.3±9.1) mmHg (1 mmHg=0.133 kPa) vs(116.9±10.8) mmHg, (80.0±8.6) mmHg vs (77.0±8.0) mmHg; Z=4.08, 2.24, all P<0.05]. HRV indices, including the standard deviation of normal to normal interval (SDNN), root mean square of successive differences (RMSSD), total power (TP), low frequency (LF), and high frequency (HF), were significantly lower in the trauma group [25.3 (19.4, 30.4) me vs 36.3 (27.4, 49.0) ms, 18.3 (12.9, 27.2) me vs 26.2 (19.0, 38.5) ms, 6.0(5.4, 6.5)ms 2vs 7.0(6.3, 7.4)ms 2,4.4(3.7,5.3)ms 2vs 5.8(4.9,6.3)ms 2, 4.2(3.4, 5.2)ms 2vs 5.2(4.6, 6.1)ms 2, respectively; all P<0.001]. Spearman correlation analysis showed that childhood trauma experiences in patients with depression were positively correlated with resting systolic blood pressure and diastolic blood pressure ( r=0.309, 0.236; P<0.01), childhood trauma was negatively correlated with HRV (SDNN, RMSSD, TP, LF, HF) ( r=-0.264, -0.274, -0.271, -0.235, -0.279; all P<0.01). Multiple linear regression analysis showed that childhood trauma was positively correlated with resting-state systolic blood pressure and resting-state diastolic blood pressure ( β=0.305, 0.291; all P<0.001). Childhood trauma was negatively correlated with RMSSD, TP, LF, and HF( β=-0.244, -0.249, -0.233, -0.263; all P<0.01). Mediation effect analysis showed that parasympathetic activity partially mediated the relationship between childhood trauma and resting systolic blood pressure (effect size 0.04, standard error 0.02, 95% CI=0.01-0.09), accounting for 14.29% (0.04/0.28) of the total effect. Conclusion:Childhood trauma experiences are associated with elevated resting blood pressure and reduced HRV in patients with depression. Decreased parasympathetic activity partially mediates the relationship between childhood trauma and elevated resting systolic blood pressure in these patients.

Objective:To evaluate the role of the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-tumor necrosis factor receptor-associated factor 6 (TRAF6) signaling pathway in the reduction of cerebral ischemia-reperfusion injury (CIRI) by trilobatin pretreatment in rats.Methods:Eighty clean-grade healthy male Sprague-Dawley rats, aged 8 weeks, weighing 250-300 g, were divided into 4 groups ( n=20 each) using a random number table method: sham operation group (group S), group CIRI, trilobatin+ CIRI group (group TC) and trilobatin+ CIRI+ AAV-TLR4 group (group TCA). The model of CIRI was established by middle cerebral artery occlusion in anesthetized animals in CIRI, TC and TCA groups. In group TCA, the adeno associated virus was injected into the cortical region to up-regulate the expression of TLR4 at 21 days before developing the model. Trilobatin 15 mg/kg was administered by gavage twice daily for 3 days prior to ischemia in TC and TCA groups. The cognitive function was assessed using the modified Longa score at 24 h of reperfusion. Then the rats were sacrificed and the whole brain tissues were isolated for determination of the cerebral infarct size (by TTC staining), expression of TLR4, MyD88 and TRAF6 (by Western blot), and contents of interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) (by enzyme-linked immunosorbent assay) and for microscopic examination of the neuronal ultrastructure in ischemic cerebral cortex tissues (with a transmission electron microscope). Results:Compared with group S, the Longa score and percentage of cerebral infarct size were significantly increased, the expression of TLR4, MyD88 and TRAF6 in cerebral cortex tissues of ischemic regions was up-regulated, the contents of IL-1β, IL-6 and TNF-α were increased ( P<0.05), and the pathological damage to cortical neurons was aggravated in CIRI group. Compared with group CIRI, the Longa score and percentage of cerebral infarct size were significantly decreased, the expression of TLR4, MyD88 and TRAF6 was down-regulated, the contents of IL-1β, IL-6 and TNF-α were decreased in cerebral cortex tissues of ischemic regions ( P<0.05), and the pathological damage to cortical neurons was significantly attenuated in group TC. Compared with group TC, the Longa score and percentage of cerebral infarct size were significantly increased, the expression of TLR4, MyD88 and TRAF6 was up-regulated, the contents of IL-1β, IL-6 and TNF-α were increased in cerebral cortex tissues of ischemic regions ( P<0.05), and the pathological damage to cortical neurons was aggravated in group TCA. Conclusions:The TLR4-MyD88-TRAF6 signaling pathway is involved in the reduction of cerebral I/R injury by trilobatin pretreatment in rats.

Objective:To evaluate the role of the Toll-like receptor 4 (TLR4)-myeloid differentiation factor 88 (MyD88)-tumor necrosis factor receptor-associated factor 6 (TRAF6) signaling pathway in the reduction of cerebral ischemia-reperfusion injury (CIRI) by trilobatin pretreatment in rats.Methods:Eighty clean-grade healthy male Sprague-Dawley rats, aged 8 weeks, weighing 250-300 g, were divided into 4 groups ( n=20 each) using a random number table method: sham operation group (group S), group CIRI, trilobatin+ CIRI group (group TC) and trilobatin+ CIRI+ AAV-TLR4 group (group TCA). The model of CIRI was established by middle cerebral artery occlusion in anesthetized animals in CIRI, TC and TCA groups. In group TCA, the adeno associated virus was injected into the cortical region to up-regulate the expression of TLR4 at 21 days before developing the model. Trilobatin 15 mg/kg was administered by gavage twice daily for 3 days prior to ischemia in TC and TCA groups. The cognitive function was assessed using the modified Longa score at 24 h of reperfusion. Then the rats were sacrificed and the whole brain tissues were isolated for determination of the cerebral infarct size (by TTC staining), expression of TLR4, MyD88 and TRAF6 (by Western blot), and contents of interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor-alpha (TNF-α) (by enzyme-linked immunosorbent assay) and for microscopic examination of the neuronal ultrastructure in ischemic cerebral cortex tissues (with a transmission electron microscope). Results:Compared with group S, the Longa score and percentage of cerebral infarct size were significantly increased, the expression of TLR4, MyD88 and TRAF6 in cerebral cortex tissues of ischemic regions was up-regulated, the contents of IL-1β, IL-6 and TNF-α were increased ( P<0.05), and the pathological damage to cortical neurons was aggravated in CIRI group. Compared with group CIRI, the Longa score and percentage of cerebral infarct size were significantly decreased, the expression of TLR4, MyD88 and TRAF6 was down-regulated, the contents of IL-1β, IL-6 and TNF-α were decreased in cerebral cortex tissues of ischemic regions ( P<0.05), and the pathological damage to cortical neurons was significantly attenuated in group TC. Compared with group TC, the Longa score and percentage of cerebral infarct size were significantly increased, the expression of TLR4, MyD88 and TRAF6 was up-regulated, the contents of IL-1β, IL-6 and TNF-α were increased in cerebral cortex tissues of ischemic regions ( P<0.05), and the pathological damage to cortical neurons was aggravated in group TCA. Conclusions:The TLR4-MyD88-TRAF6 signaling pathway is involved in the reduction of cerebral I/R injury by trilobatin pretreatment in rats.

Objective:To explore the effects of childhood trauma on resting blood pressure, heart rate, and heart rate variability in patients with depression.Methods:A cross-sectional study was designed to prospectively collect clinical data on a total of 163 patients with depression, including 47 males and 116 females, aged 18-50 years,with mean[ M( Q1, Q3)] [29.0, (21.0, 37.0)]years, who were either the outpatients or the inpatients in the Mental Health Center of the First Hospital of Hebei Medical University from September 2022 to June 2024. The Childhood Trauma Questionnaire-Short form (CTQ-SF) was used to assess the experience of abuse and neglect during childhood. According to the CTQ-SF score, the subjects were divided into a trauma group ( n=80) and a non-trauma group ( n=83). The 17-item Hamilton Depression Scale (HAMD 17) and Hamilton Anxiety Scale (HAMA) were used to assess depressive and anxiety symptoms in the participants, respectively. A digital blood pressure monitor and an autonomic nervous system response detector were employed to measure resting blood pressure, heart rate, and heart rate variability (HRV). Spearman correlation analysis was used to examine the relationships between childhood trauma and resting blood pressure, heart rate, and HRV. Multiple linear regression analysis was performed to analyze factors influencing these parameters. The Bootstrap method was employed to test the potential mediating role of parasympathetic nervous system activity in the relationships between childhood trauma and resting blood pressure, and heart rate. Results:No significant difference was observed in resting heart rate between the trauma and non-trauma groups ( P>0.05). However, the trauma group exhibited higher resting systolic and diastolic blood pressure [(123.3±9.1) mmHg (1 mmHg=0.133 kPa) vs(116.9±10.8) mmHg, (80.0±8.6) mmHg vs (77.0±8.0) mmHg; Z=4.08, 2.24, all P<0.05]. HRV indices, including the standard deviation of normal to normal interval (SDNN), root mean square of successive differences (RMSSD), total power (TP), low frequency (LF), and high frequency (HF), were significantly lower in the trauma group [25.3 (19.4, 30.4) me vs 36.3 (27.4, 49.0) ms, 18.3 (12.9, 27.2) me vs 26.2 (19.0, 38.5) ms, 6.0(5.4, 6.5)ms 2vs 7.0(6.3, 7.4)ms 2,4.4(3.7,5.3)ms 2vs 5.8(4.9,6.3)ms 2, 4.2(3.4, 5.2)ms 2vs 5.2(4.6, 6.1)ms 2, respectively; all P<0.001]. Spearman correlation analysis showed that childhood trauma experiences in patients with depression were positively correlated with resting systolic blood pressure and diastolic blood pressure ( r=0.309, 0.236; P<0.01), childhood trauma was negatively correlated with HRV (SDNN, RMSSD, TP, LF, HF) ( r=-0.264, -0.274, -0.271, -0.235, -0.279; all P<0.01). Multiple linear regression analysis showed that childhood trauma was positively correlated with resting-state systolic blood pressure and resting-state diastolic blood pressure ( β=0.305, 0.291; all P<0.001). Childhood trauma was negatively correlated with RMSSD, TP, LF, and HF( β=-0.244, -0.249, -0.233, -0.263; all P<0.01). Mediation effect analysis showed that parasympathetic activity partially mediated the relationship between childhood trauma and resting systolic blood pressure (effect size 0.04, standard error 0.02, 95% CI=0.01-0.09), accounting for 14.29% (0.04/0.28) of the total effect. Conclusion:Childhood trauma experiences are associated with elevated resting blood pressure and reduced HRV in patients with depression. Decreased parasympathetic activity partially mediates the relationship between childhood trauma and elevated resting systolic blood pressure in these patients.

Objective:To evaluate the role of the SIRT1/FoxO1 signaling pathway in trilobatin-induced reduction of cerebral ischemia-reperfusion (I/R) injury in rats.Methods:Eighty clean-grade healthy male Sprague-Dawley rats, aged 6-8 weeks, weighing 230-280 g, were divided into 4 groups ( n=20 each) using a random number table method: sham operation group (group S), cerebral I/R group (group CIR), trilobatin+ cerebral I/R group (group T) and trilobatin+ cerebral I/R+ SIRT1/FoxO1 signaling pathway inhibitor EX527 group (group E). The model of focal cerebral I/R injury was established by middle cerebral artery occlusion in anesthetized animals. Trilobatin 15 mg/kg was given by gavage twice a day for 3 consecutive days starting from 3 days before ischemia in T and E groups. EX527 5 mg/kg was intraperitoneally injected before each gavage in group E. Modified Longa scoring scale was used to assess neurological function at 24 h of reperfusion, then the rats were sacrificed and whole brain tissues were obtained for determination of cerebral infarct size (using TTC staining), apoptosis rate and level of reactive oxygen species (ROS) in the hippocampus (by flow cytometry), expression of SIRT1 and acetylated FOXO1 (Ac-FOXO1) (by Western blot) and contents of superoxide dismutase (SOD) and malondialdehyde (MDA) (by enzyme-linked immunosorbent assay) and for microscopic examination of pathological changes in the hippocampal CAI area after HE staining. Results:Compared with group S, Longa score, cerebral infarct size, apoptosis rate of hippocampal neurons, and levels of ROS and MDA were significantly increased, the content of SOD was decreased, the expression of SIRT1 was down-regulated, and the expression of Ac-FOXO1 was up-regulated in group CIR ( P<0.05). Compared with group CIR, Longa score, cerebral infarct size, apoptosis rate of hippocampal neurons, and levels of ROS and MDA were significantly decreased, the content of SOD was increased, the expression of SIRT1 was up-regulated, and the expression of Ac-FOXO1 was down-regulated in group T ( P<0.05). Compared with group T, Longa score, cerebral infarct size, apoptosis rate of hippocampal neurons, and levels of ROS and MDA were significantly increased, the content of SOD was decreased, the expression of SIRT1 was down-regulated, and the expression of Ac-FOXO1 was up-regulated in group E ( P<0.05). Conclusions:Trilobatin may inhibit oxidative stress responses and neuronal apoptosis in hippocampi by activating the SIRT1/FoxO1 signaling pathway, thus alleviating cerebral I/R injury in rats.

Objective:To develop a perinatal depression screening scale for Chinese urban version and test its reliability and validity.Methods:Naturally conceived women who were≥12 weeks of gestation and had regular prenatal examinations or delivered within four weeks in Xi'an and Foshan were recruited using convenience sampling. Initial entries were created through clinical interviews and expert validation of 50 of these pregnancies. Further item screening and testing for reliability and validity using correlation analysis, critical ratio method, homogeneity test, and factor analysis were performed. The final questionnaire was formed and then used to test the subjects. Fifty women who had completed the questionnaire effectively were selected for retesting 10 to 15 days after the initial evaluation. A structural equation model was constructed using the Edinburgh Postpartum Depression Scale (EPDS) as the reference criterion to conduct the scale's exploratory and confirmatory factor analysis. The receiver operating characters curve was used to determine the cut-off point of the scale.Results:(1) 1 300 questionnaires were issued, and 1 049 valid questionnaires were received with a recovery rate of 80.7%. Among them, 601 were used for exploratory and correlation analysis, and 448 were used for confirmatory factor analysis. (2) The initial entries of the scale totaled 63. After eliminating indicators that did not meet the requirements for item analysis, the final scale consisted of 22 entries in total. The final scale consisted of six dimensions, including "abnormal mood", "loss of interest and pleasure," "sleep disorder," "self-blame and guilt," "decline in conscious thought ability," and "lack of energy". (3) The correlation coefficients between the above six dimensions and EPDS were 0.609, 0.322, 0.423, 0.522, 0.545, and 0.516, respectively. The one between the total scale and EPDS was 0.715 (all P<0.01). (4) The confirmatory factor analysis of each model and the scale showed an acceptable fit and a stable factor structure with indices Chi-square/degrees of freedom =2.504, square root of approximation error=0.058, standardized root mean square residual=0.048, comparative fit index=0.925, Tueker-Lewis index=0.911. After retaining 22 items, the Cronbach's coefficients of the six dimensions ranged from 0.708 to 0.870. (5) The test-retest reliability of the total scale, six dimensions, and 22 items were 0.936, 0.786-0.846, and 0.720-0.886, respectively. (6) The receiver operating characteristic curve of the scale was drawn with EPDS≥13 as the cut-off value, and the area under the curve (AUC) of EPDS was 0.808 (95% CI: 0.744-0.872). When the original cut-off point was 21, the Youden index was the max (0.561), with sensitivity and specificity of 0.952 and 0.609, respectively. The Kappa value was 0.691, indicating that the scale was consistent with EPDS. Conclusion:This study preliminarily established a Chinese urban version of the perinatal depression screening scale with a stable factor structure and good reliability and validity.

Objective:To develop a perinatal depression screening scale for Chinese urban version and test its reliability and validity.Methods:Naturally conceived women who were≥12 weeks of gestation and had regular prenatal examinations or delivered within four weeks in Xi'an and Foshan were recruited using convenience sampling. Initial entries were created through clinical interviews and expert validation of 50 of these pregnancies. Further item screening and testing for reliability and validity using correlation analysis, critical ratio method, homogeneity test, and factor analysis were performed. The final questionnaire was formed and then used to test the subjects. Fifty women who had completed the questionnaire effectively were selected for retesting 10 to 15 days after the initial evaluation. A structural equation model was constructed using the Edinburgh Postpartum Depression Scale (EPDS) as the reference criterion to conduct the scale's exploratory and confirmatory factor analysis. The receiver operating characters curve was used to determine the cut-off point of the scale.Results:(1) 1 300 questionnaires were issued, and 1 049 valid questionnaires were received with a recovery rate of 80.7%. Among them, 601 were used for exploratory and correlation analysis, and 448 were used for confirmatory factor analysis. (2) The initial entries of the scale totaled 63. After eliminating indicators that did not meet the requirements for item analysis, the final scale consisted of 22 entries in total. The final scale consisted of six dimensions, including "abnormal mood", "loss of interest and pleasure," "sleep disorder," "self-blame and guilt," "decline in conscious thought ability," and "lack of energy". (3) The correlation coefficients between the above six dimensions and EPDS were 0.609, 0.322, 0.423, 0.522, 0.545, and 0.516, respectively. The one between the total scale and EPDS was 0.715 (all P<0.01). (4) The confirmatory factor analysis of each model and the scale showed an acceptable fit and a stable factor structure with indices Chi-square/degrees of freedom =2.504, square root of approximation error=0.058, standardized root mean square residual=0.048, comparative fit index=0.925, Tueker-Lewis index=0.911. After retaining 22 items, the Cronbach's coefficients of the six dimensions ranged from 0.708 to 0.870. (5) The test-retest reliability of the total scale, six dimensions, and 22 items were 0.936, 0.786-0.846, and 0.720-0.886, respectively. (6) The receiver operating characteristic curve of the scale was drawn with EPDS≥13 as the cut-off value, and the area under the curve (AUC) of EPDS was 0.808 (95% CI: 0.744-0.872). When the original cut-off point was 21, the Youden index was the max (0.561), with sensitivity and specificity of 0.952 and 0.609, respectively. The Kappa value was 0.691, indicating that the scale was consistent with EPDS. Conclusion:This study preliminarily established a Chinese urban version of the perinatal depression screening scale with a stable factor structure and good reliability and validity.

Objective To study the clinical effect of Yaotongning capsule combined with etoricoxib for the pain and inflammation of lumbar vertebrae in elderly patients with lumbar osteoarthritis. Methods 120 elderly patients with lumbar osteoarthritis admitted to our hospital from January 2016 to June 2018 were randomly divided into the control group and the observation group, with 60 patients in each group. Patients in the control group were treated with etoricoxib, while patients in the observation group were treated with etoricoxib plus Yaotongning capsule orally. Both groups received medications for 2 weeks. Spinal pain and quality of life score changes were recorded. The inflammatory cytokines in serum TNF-α, GM-CSF, COX-2 and BMP-2 levels were monitored. The clinical efficacy was compared and drug safety profile was evaluated for two groups. Results The effective rates of the control group and the observation group were 78.33% and 91.67% respectively. The effective rate in the observation group weas significantly higher (P<0.05). After treatment, the VAS score for the patients in the observation group was significantly lower than that in the control group (P<0.05). The SF-36 score in the observation group was significantly increased (P<0.05), and the levels of TNF-α,GM-CSF and COX-2 in the serum were significantly lower than those in the control group (P<0.05), and the levels of BMP-2 were significantly increased (P<0.05). Conclusion Yaotongning capsule combined with etoricoxib in the treatment of senile lumbar osteoarthritis has definite curative effect. It significantly reduced lumbar pain, improved quality of life, inhibited inflammatory reaction, and had a better drug safety profile. The further clinical investigation for the combination therapy is warranted.

Objective: To compare the efficacy of femoral triangle versus adductor canal approach to saphenous nerve block for postoperative analgesia in the patients undergoing knee arthroplasty. Methods: Sixty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients of both sexes, aged 53-68 yr, scheduled for elective total knee arthroplasty under general anesthesia, were assigned into 2 groups (n=30 each) using a random number table method: femoral triangle approach to saphenous nerve block group (group F) and adductor canal approach to saphenous nerve block group (group A). Femoral triangle and adductor canal approach to saphenous nerve block was performed by injecting 0.5% ropivacaine 20 ml in group F and group A, respectively.Patient-controlled saphenous nerve block analgesia was used in two groups, and the analgesic pump solution contained 1% ropivacaine 400 mg diluted to 160 ml in 0.9% sodium chloride injection.The analgesic pump was set up with a 5 ml bolus dose, a 30-min lockout interval and background infusion at a rate of 5 ml/h, and analgesia lasted until 72 h after operation.When visual analog scale score > 4 and pain was not relived after 30-min pressing by patients, pethidine hydrochloride 100 mg was intramuscularly injected as rescue analgesic.The muscle strength of quadriceps femoris was assessed by manual muscle test at 4, 8, 24, 48 and 72 h after operation.The patient′s satisfaction score was assessed and recorded at 72 h after operation.Rescue analgesia and development of adverse reactions (local anesthetic intoxication, itching, dizziness, urinary retention, nausea and vomiting) were recorded within 72 h after operation. Results: Compared with group F, the muscle strength of quadriceps femoris was significantly increased at 4, 8 and 24 h after operation, the rate of postoperative rescue analgesia was decreased (P<0.05), and no significant change was found in patient′s satisfaction score or incidence of adverse reactions in group A (P>0.05). Conclusion Adductor canal approach to saphenous nerve block provides better efficacy for postoperative analgesia than femoral triangle approach to saphenous nerve block in the patients undergoing knee arthroplasty.