BACKGROUND:Formononetin is an isoflavonoid compound widely found in red clover,astragalus,and chickweed,which has the ability to inhibit oxidative stress,inflammatory factor release,and apoptosis. OBJECTIVE:To investigate the effect of formononetin on interleukin-1β-induced chondrocyte injury and its mechanism. METHODS:(1) Cartilage tissues from patients with osteoarthritis and patients with simple meniscus injury were collected,and real-time quantitative PCR was used to detect miR-135b-5p expression. (2) Human chondrocytes were cultured in vitro,and then divided them into nine groups:cells in normal control group were cultured for 48 hours with no treatment;cells in interleukin-1β group were treated with interleukin-1β for 48 hours;cells in interleukin-1β+low-dose formononetin group were treated with 25 μmol/L formononetin for 24 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+middle-dose formononetin group were treated with 50 μmol/L formononetin for 24 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+high-dose formononetin group were treated with 100 μmol/L formononetin for 24 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+miR NC group were treated with miR NC for 6 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+miR-135b-5p group were treated with miR-135b-5p mimics for 6 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+high dose formononetin+anti-miR-NC group were treated with anti-miR-NC for 6 hours,then treated with 100 μmol/L formononetin for 24 hours,and finally treate with interleukin-1β for 48 hours;cells in interleukin-1β+high-dose formononetin+anti-miR-135b-5p group were treated with anti-miR-135b-5p for 6 hours,the treated with 100 μmol/L formononetin for 24 hours,and finally treated with interleukin-1β for 48 hours. Relevant tests are performed after treatment. RESULTS AND CONCLUSION:The expression level of miR-135b-5p in cartilage tissue of patients with osteoarthritis was significantly lower than that of patients with simple meniscus injury (P<0.05). Compared with the normal control group,the expression level of miR-135b-5p,proliferative ability,activity of superoxid dismutase,and expression levels of collagenase Ⅱ protein and Bcl-2 protein in chondrocytes were lower in the interleukin-1β group (P<0.05),while apoptotic rate,lactate dehydrogenase activity,malondialdehyde level,levels of proinflammatory factors,and expression levels of matrix metalloproteinase-13 protein and Bax protein were higher in the interleukin-1β group (P<0.05). Formononetin inhibited chondrocyte damage caused by interleukin-1β in a concentration-dependent manner. Transfection of miR-135b-5p mimics elevated miR-135b-5p expression in the interleukin-1β group and inhibited chondrocyte damage induced by interleukin-1β;transfection of anti-miR-135b-5p decreased miR-135b-5p expression in the interleukin-1β+high-dose formononetin group and inhibited the effect of formononetin on chondrocytes. To conclude,the protective effect of formononetin on chondrocyte injury induced by interleukin-1β may be related to the regulation of miR-135b-5p expression.

BACKGROUND:Formononetin is an isoflavonoid compound widely found in red clover,astragalus,and chickweed,which has the ability to inhibit oxidative stress,inflammatory factor release,and apoptosis. OBJECTIVE:To investigate the effect of formononetin on interleukin-1β-induced chondrocyte injury and its mechanism. METHODS:(1) Cartilage tissues from patients with osteoarthritis and patients with simple meniscus injury were collected,and real-time quantitative PCR was used to detect miR-135b-5p expression. (2) Human chondrocytes were cultured in vitro,and then divided them into nine groups:cells in normal control group were cultured for 48 hours with no treatment;cells in interleukin-1β group were treated with interleukin-1β for 48 hours;cells in interleukin-1β+low-dose formononetin group were treated with 25 μmol/L formononetin for 24 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+middle-dose formononetin group were treated with 50 μmol/L formononetin for 24 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+high-dose formononetin group were treated with 100 μmol/L formononetin for 24 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+miR NC group were treated with miR NC for 6 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+miR-135b-5p group were treated with miR-135b-5p mimics for 6 hours followed by treatment with interleukin-1β for 48 hours;cells in interleukin-1β+high dose formononetin+anti-miR-NC group were treated with anti-miR-NC for 6 hours,then treated with 100 μmol/L formononetin for 24 hours,and finally treate with interleukin-1β for 48 hours;cells in interleukin-1β+high-dose formononetin+anti-miR-135b-5p group were treated with anti-miR-135b-5p for 6 hours,the treated with 100 μmol/L formononetin for 24 hours,and finally treated with interleukin-1β for 48 hours. Relevant tests are performed after treatment. RESULTS AND CONCLUSION:The expression level of miR-135b-5p in cartilage tissue of patients with osteoarthritis was significantly lower than that of patients with simple meniscus injury (P<0.05). Compared with the normal control group,the expression level of miR-135b-5p,proliferative ability,activity of superoxid dismutase,and expression levels of collagenase Ⅱ protein and Bcl-2 protein in chondrocytes were lower in the interleukin-1β group (P<0.05),while apoptotic rate,lactate dehydrogenase activity,malondialdehyde level,levels of proinflammatory factors,and expression levels of matrix metalloproteinase-13 protein and Bax protein were higher in the interleukin-1β group (P<0.05). Formononetin inhibited chondrocyte damage caused by interleukin-1β in a concentration-dependent manner. Transfection of miR-135b-5p mimics elevated miR-135b-5p expression in the interleukin-1β group and inhibited chondrocyte damage induced by interleukin-1β;transfection of anti-miR-135b-5p decreased miR-135b-5p expression in the interleukin-1β+high-dose formononetin group and inhibited the effect of formononetin on chondrocytes. To conclude,the protective effect of formononetin on chondrocyte injury induced by interleukin-1β may be related to the regulation of miR-135b-5p expression.

Objective:To investigate the clinical characteristics of the severe trauma patients with Acute kidney injury (AKI) ,and analyze the risk factors and clinical prognosis.Methods:Clinical data of severe trauma patients admitted to ICU of Xiaolan Hospital of Southern Medical University, from July 2018 to December 2020 were retrospectively analyzed. Demographic data, basic diseases, critical disease score, serum creatinine, hemoglobin, treatment options, blood transfusion volume, and clinical outcomes were collected to establish a clinical database. AKI was diagnosed and graded according to the Kidney Disease Improving Global Outcomes (KDIGO) criterion, and trauma type was classified according to the main injury part. The clinical data and laboratory examination of different groups were compared to analyze the clinical characteristics and prognosis in severe trauma patients. The risk factors of AKI in severe trauma patients were analyzed by Logistic regression.Results:(1) A total of 175 patients with severe trauma were eligible for inclusion, and the incidence of AKI was 30.9%(54/175), including 29 patients with AKI stage 1(16.6%), 15 patients with AKI stage 2 (8.6%), and 10 patients with AKI stage 3 (5.7%). In the cohort, the rate of in-hospital renal replacement therapy was 4%, in-hospital mortality was 5.7%, and 28-day mortality was 16.6%. (2) The age, shock patients, ICU admission serum creatinine, APACHEⅡscore and ISS score of AKI group were significantly higher than those of non-AKI group ( P<0.05). There were no significant differences between the two groups in gender, underlying diseases (hypertension and diabetes), ICU admission hemoglobin level and contrast agent utilization rate( P>0.05). Compared with the non-AKI group, AKI group had higher rates of surgical treatment (63% vs. 44.6%), more blood transfusion [875(720,1110)mL & 670(610,750)mL], longer ICU stay [6(4,11)d & 4(2.5,7.5)d], and higher rates of mechanical ventilation (96.3% vs. 81%), renal replacement therapy rate (13% vs. 0), in-hospital mortality (13% vs. 2.5%) and 28-day mortality (25.9% vs. 12.4%), the differences were statistically significant ( P<0.05). (3) The incidence of AKI was different in patients with different types of severe trauma, and the abdominal trauma group with a highest rate (50%). The serum creatinine at ICU admission and the peak value during hospitalization in abdominal trauma group were significantly higher than those in other injury types ( P<0.05). (4) Logistic regression analysis showed Age [ OR=1.020, 95% CI(1.003,1.038), P=0.024], APACHEⅡscore [ OR=1.137, 95% CI(1.053,1.228), P=0.001], shock [ OR=1.102, 95% CI(0.906,1.208), P=0.034], ICU admission serum creatinine [ OR=1.068, 95% CI(1.036,1.102), P=0.000], surgical treatment [ OR=4.205, 95% CI(1.446,12.233), P=0.008], blood transfusion volume [ OR=1.006, 95% CI(1.002,1.009), P=0.001] were independent risk factors for AKI in severe trauma patients. Conclusions:Severe trauma patients yield a high incidence of AKI influencing clinical prognosis. The incidence of AKI varies with different types of severe trauma. Age, APACHEⅡscore, shock, ICU admission serum creatinine, surgical treatment, and blood transfusion volume are independent risk factors for AKI in severe trauma patients.

Objective:To investigate the clinical value of neuron specific enolase (NSE) and bispectral index (BIS ) in predicting the neurological prognosis in patients with severe intracerebral hemorrhage.Methods:Patients with severe intracerebral hemorrhage admitted to the ICU of Xiaolan Hospital of Southern Medical University from January 2019 to December 2020 were selected, and serum NSE detection and BIS monitoring were performed at an early stage. According to the Glasgow outcome scale (GOS) at 90 days after intracerebral hemorrhage, the patients were divided into the good neurologic prognosis group (GOS 4-5) and poor neurologic prognosis group (GOS 1-3). The levels of NSE and BIS between the two groups were compared. Receiver operating characteristic (ROC) curve and area under the curve (AUC) were used to evaluate the predictive value of NSE, BIS and their combination in predicting neurological prognosis.Results:A total of 126 patients with severe intracerebral hemorrhage were enrolled in this study, and 32 patients (25.4%) had poor neurological prognosis. The level of NSC in the poor neurological prognosis group was significantly higher than that in the good neurologic prognosis group [28 (13.7, 50.4) ng/mL vs. 13.5 (9.6, 18.5) ng/mL, P < 0.05], while the BIS level was significantly lower than that in the good neurologic prognosis group [32 (25.2, 45) vs. 55 (48, 62.2), P <0.05]. For detection of poor neurologic outcome in patients with severe intracerebral hemorrhage, NSE and BIS yielded the AUC values of 0.768 (0.685, 0.839) and 0.866 (0.793, 0.920), respectively, with cut-off values of 21.7 ng/mL and 47, respectively. The combination of NSE and BIS yielded a remarkably higher AUC value of 0.927 (0.867, 0.966) for predicting poor neurologic outcome than each index alone ( P<0.05). Conclusions:Early monitoring of NSE and BIS can effectively predict the neurological prognosis of patients with severe intracerebral hemorrhage, and the combination of NSE and BIS can further improve the prediction efficiency.

OBJECTIVE To explore the antidepressant effect and the underlying mechanisms of schisandrin (SCH), a component of the fruits of Schizandra chinesis. METHODS The forced swimming test (FST) and tail suspension test (TST) in mice were used to evaluate the antidepressant activity of SCH (5, 10, and 30 mg · kg-1) following single administration intragastrically, and the locomotor activity was investigated to exclude its neural excitatory effects. Effects of SCH on neural monoamine systems were studied in two pharmacological models, including reserpine induced monoamine depletion test and yohimbine toxicity potentiation test. RESULTS In behavioral despair models, SCH (30 mg·kg-1) signif?icantly decreased the immobility time in the TST and FST (P<0.05) compared with normal control group. Results of the locomotor activity experiment showed that SCH had no excitatory or inhibitory actions on the central nervous system. In the reserpine reversal experiment, SCH (30 mg · kg-1) antagonized thepalpebral ptosis and akinesia symptoms caused by reserpine(2.5 mg · kg-1) treatment (P<0.05) compared with model group, but had little effect on the drop of the anal temperature. Moreover, SCH did not increase the lethality caused by subcutaneous injection of yohimbine (30 mg · kg-1)at the threshold lethal dosage. CONCLUSION SCH exerts potential antidepressant-like effect in mice.

Objective To explore the HEART risk score in predicting 30-day major adverse cardiovascu-lar events (MACE)for the patients presenting to Emergency Department (ED) with acute chest pain. Methods Patients presented in our ED with acute chest pain were enrolled from January,2016 to April,2016. All cause MACE of each patient were followed up at 30 days by Health insurance information management System and call . Results Total 209 patients were enrolled(mean age 65.28 ± 16.85 years;52.63%male). The age,hypertension, ratio of ACS,SpO2,in-patient number HEART score in MACE subject were significantly higher than that in non MACE patients(P<0.05). The blood pressure at admission of MACE patients was significantly decrease than that in non MACE patients(P<0.05). The MACE within 30 days was 5.74%. The respective areas under the curve (AUC)for 30-day MACE(95% CI)was 0.908(0.846 ~ 0.974). The percent of patients with 30-day MACE with HEART scores between 0% and 3,4 ~ 6,and 7 ~ 10 was 0%,2.5%,and 27%,respectively. Conclusion HEART score can be simple,rapid and accurate prediction of emergency department of patients with acute chest pain within 30 days of MACE,effective elimination of low-risk patients with MACE,it plays a very important role for disease assessment and diagnosis and treatment process in emergency department.

Objective To evaluate the diagnostic performance of a point-of-care testing for sensitive cardiac troponin Ⅰ (POCT-cTnI) in early diagnosis of chest pain patients who had a high pretest probability of acute myocardial infarction (AMI).Methods Total of 127 patients with new-onset chest pain at the emergency department were enrolled.Blood samples were drawn for the routine blood test,and determined POCT-cTnI and central laboratory testing for high sensitive cardiac troponin T (CLT-hscTnT) at admission,three and then at six hours after admission.All patients were divided into AMI group and non-AMI group according to the final diagnosis,which was adjudicated independently by two physicians who reviewed all available medical records for the 90-day follow-up period,and they were unaware of the results of the investigational assays of cardiac troponins.The receiver operating characteristic (ROC) curves were constructed to assess and compare the diagnostic performance of AMI of two cardiac troponin assays.The comparison of areas under the ROC curves (AUC) was performed by DeLong test,and the sensitivity,specificity,negative predictive values (NPV) and positive predictive values (PPV) for the target markers were calculated by applying a maker-specific cutoff value.Results The final diagnosis of AMI was made in 40 of 127 patients (31.5 ％).The diagnostic accuracy of the two assays oBtained at presentation,as quantified by AUC,was no statistically differences (AUC for POCT-cTnⅠ,0.901,95％ CI,0.901 to 0.947;and for CLT-hscTnT,0.907,95％ CI,0.842 to 0.951;Z =0.235,P =0.745).The AUC for POCT-cTnI at 3 hours after admission was significantly higher than that on admission (0.931 vs.0.858;Z =-2.038,P =0.042),while there was on further improvement at 6 hours after admission (0.931 vs.0.949;Z =-1.435,P =0.151).With use of POCT-cTnI (cutoff value 0.023 ng/mL,which was the 99th percentile upper reference limit) on adimission,the clinical sensitivity was 77.5％,and the specificity was 94.2％.A single sample of POCT-cTnI at 3 hours after admission improved the diagnostic accuracy,with a sensitivity of 96.4％,a specificity of 92.0％,and a NPV of 98.6％,a PPV of 81.8％.While,with use of CLT-hscTnT (cutoff value 0.014 ng/mL,was the 99th percentile upper reference limit) at 3 hours after admission,the NPV reached to 100％.Conclusions The use of a POCT-cTnI assay in chest pain patients can identify and exclude the AMI rapidly and exactly at three hours after admission,and the diagnostic performance is equivalent to CLT-hscTnT.