Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Background: Acetaminophen (APAP)-induced hepatotoxicity has attracted considerable attention in clinical settings due to the limited treatment options available. Liensinine stands out as a key alkaloid known for its pharmaceutical activities. However, the role of liensinine in mitigating APAP-induced liver injury remains unclear. Objective: The aim of the study was to explore the protective effects of liensinine against APAP-induced liver injury. Methods: C57BL/6 male mice were treated with a dose of 200 mg/kg N-acetylcysteine or varying doses of liensinine (10 or 20 mg/kg) for seven consecutive days. APAP (400 mg/kg, i.g.) was then administered to induce liver damage for 12 hours. Blood samples and hepatic tissues were collected for further analysis. Liver enzyme levels and histopathological analysis were employed to assess liver injury. RNA-seq was conducted to evaluate the dynamic changes in gene expression. Biochemical assays were used to measure oxidative stress and inflammation, while the TUNEL assay was performed to assess hepatocyte apoptosis. Results: The results demonstrated that the administration of liensinine mitigated serum liver enzyme levels and tissue damage resulting from APAP overdose. Transcriptome analysis revealed significant and coordinated changes in genes related to the peroxisome proliferator-activated receptor signaling pathway, mitogen-activated protein kinase signaling pathway, and apoptosis pathway in response to APAP-induced hepatotoxicity. The expression alterations of key genes within these three pathways, associated with inflammation, oxidative stress, and cell apoptosis, were reversed by liensinine, indicating its potential in alleviating APAP-induced liver damage through multiple signaling pathways. This suggests the diverse therapeutic effects of liensinine, including inflammation suppression, oxidative stress reduction, and cell apoptosis inhibition. Indeed, pretreatment with liensinine effectively reduced inflammatory cytokines, oxidative stress indicators, and apoptotic cells induced by APAP. Conclusions: Liensinine mitigates APAP-induced hepatotoxicity in mice through multifaceted pathways, providing anti-inflammatory, antioxidant, and anti-apoptotic benefits.

Objective:To investigate the relationship between central venous-arterial blood carbon dioxide partial pressure difference (Pcv-aCO 2) and left ventricular ejection fraction(LVEF) in acute myocardial infarction. Methods:Clinical data of patients with acute myocardial infarction admitted to the Intensive Care Unit of Fujian Provincial Hospital from November 2019 to October 2021 were retrospectively analyzed. LVEF was measured by bedside echocardiogram. The patients were divided into the normal LVEF group (LVEF ≥ 52%) and decreased LVEF group (LVEF < 52%) according to LVEF. The differences in general information and hemodynamic parameters between the two groups were compared. The normality of the above data was tested by the Jarque-Bera test. Correlation analysis of hemodynamic indices with LVEF was performed. Binary logistic regression was used to analyze the risk factors associated with the decrease in LVEF. The feasibility of diagnosing LVEF decline with Pcv-aCO 2 was assessed using receiver operating characteristic (ROC) curve. Results:Seventy-two patients with acute myocardial infarction were included for analysis, including 25 patients in the normal LVEF group and 47 patients in the decreased LVEF group. Pcv-aCO 2 was significantly higher in the decreased LVEF group than that in the normal LVEF group [(7.13±1.19) mmHg vs. (5.41±1.23) mmHg, P<0.01]. There was a negative correlation between LVEF and Pcv-aCO 2 ( rs= -0.740, P<0.01). The area under the ROC curve for Pcv-aCO 2 was 0.849 (95% CI: 0.758-0.939, P<0.01). The binary logistic regression analysis showed that Pcv-aCO 2 was an independent risk factor for decreased LVEF ( OR=2.251, 95% CI: 1.326-3.820). Conclusions:To a certain extent, the increase of Pcv-aCO 2 can predict the decrease of LVEF in acute myocardial infarction.

Objective To investigate the effects of enteral nutrition added with glutamine on the incidences of gastrointestinal complications,intestinal mucosal barrier function and inflammatory responses in patients with acute severe traumatic brain injury (sTBI).Methods A prospective case control study was made on 107 patients with sTBI hospitalized from January 2016 to June 2017.The patients were divided into experimental group added with glutamine (n =54) and control group without glutamine (n =53) according to the random number table.The general data of the patients were recorded.After treatment,the incidences of gastrointestinal complications in both groups were compared.The serum levels of intestinal mucosal barrier function indices,namely,diamine oxidase (DAO),Dlactate acid,and intestinal fat acid binding protein (I-FABP) were evaluated by enzymology spectrophotometer method.Meanwhile,the serum levels of C-reactive protein (CRP),tumor necrosis factor-α (TNF-α),and interleukin-6 (IL-6) were also tested with enzyme-linked immunosorbent assay (ELISA).Glasgow coma scale (GCS),acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ),and hospital stay in both groups were compared.Results The two group were comparable with respect to gender,age,injury reasons,body mass index,preoperative GCS,preoperative APACHE Ⅱ,injury type and injury time (P ＞ 0.05).The experimental group had lower incidences of stress ulcer,gastric retention and diarrhea compared with the control group 14 days after treatment (P ＜ 0.05).Within 14 days after treatment,the serum levels of DAO,D-lactate acid and I-FABP were significantly decreased in the experimental group at days 7 and 14 after treatment (P ＜ 0.05).The serum levels of CRP,TNF-α and IL-6 in the experimental group were significantly decreased after treatment (P ＜ 0.05).The experimental group had better prognosis compared with the control group (P ＜ 0.05),with higher GCS scores [(9.3 ± 0.7) points vs.(8.2 ± 0.7) points],lower APACHE Ⅱ scores [(15.3 ± 1.1) points vs.(17.7 ± 1.2) points] at day 14,and shorter hospital stay [(19.1 ± 2.2) days vs.(25.3 ± 2.4) days] (P ＜ 0.01).Conclusions Enteral nutrition added with glutamine can effectively reduce the incidence of gastrointestinal complications,as well as alleviate the intestinal mucosal barrier function damage and the inflammatory responses at early stage after sTBI,which possibly improves prognosis.

Objective To study the relationship between the severity of diastolic heart failure(DHF)and bone mineral density in the elderly. Methods Totally 80 elderly patients aged over 80 years who were tested as normal for cardiac diastolic function by Doppler tissue imaging(DTI) were selected and divided into four groups by the e/a ratio,i.e.,the normal group(n=18),the DHF 1 group(0.8≤e/a<1,n=25),the DHF 2 group (0.6≤e/a<0.8,n=22),and the DHF 3 group(e/a<0.6,n=15). And the other 20 healthy people by physical examination were set as the normal control group.All subjects underwent bone mineral density(BMD)measurement(including femoral neck,total femoral hip and lumbar vertebra 1?4) by dual energy X?ray absorptiometry. Results Bone mineral density(BMD)was significantly decreased(P<0.05)in DHF groups(DHF 1,DHF 2,and DHF 3). Bone mineral density significantly decreased along with the severity of DHF. Bone mineral density was positively correlated with the e/a ratio in the elderly with DHF(r=0.75,P<0.01). Conclusion The severity of diastolic heart failure is closely related to bone mineral density in the elderly. The severity of diastolic heart failure could predict osteoporosis.

OBJECTIVETo investigate cardiac function and myocardial perfusion during 48 h after cardiopulmonary resuscitation (CPR), further to test myocardial stunning and seek indicators for long-term survival after CPR.

METHODSAfter 4 min of untreated ventricular fibrillation, fifteen anesthetized pigs were studied at baseline and 2 h, 4 h, 24 h, and 48 h after restoration of spontaneous circulation (ROSC). Hemodynamic data, echocardiography and gated-single photon emission computed tomography myocardial perfusion images were carried out.

RESULTSMean arterial pressure (MAP), coronary perfusion pressure (CPP) and cardiac troponin I (CTNI) showed significant differences between eventual survival animals and non-survival animals at 4 h after ROSC (109.2 ± 10.7 mmHg vs. 94.8 ± 12.3 mmHg, P=0.048; 100.8 ± 6.9 mmHg vs. 84.4±12.6 mmHg, P=0.011; 1.60 ± 0.13 ug/L vs. 1.75 ± 0.10 ug/L, P=0.046). Mitral valve early-to-late diastolic peak velocity ratio, mitral valve deceleration time recovered 24 h; ejection faction and the summed rest score recovered 48 h after ROSC.

CONCLUSIONCardiac systolic and early active relaxation dysfunctions were reversible within survival animals; cardiac stunning might be potentially adaptive and protective after CPR. The recovery of MAP, CPP, and CTNI could be the indicators for long-term survival after CPR.

Animals ; Blood Pressure ; Cardiopulmonary Resuscitation ; Coronary Circulation ; Heart Arrest ; Hemodynamics ; Male ; Myocardial Contraction ; physiology ; Myocardial Stunning ; Swine ; Time Factors ; Ventricular Fibrillation