Sex differences in the management of patients with suspected acute coronary syndrome in China.

Few studies have assessed sex differences in the management of suspected acute coronary syndrome (ACS). We aimed to compare the evaluation, treatment, and outcomes between males and females with suspected ACS in the emergency department. Data were obtained from a prospective registry of acute chest pain involving 21 emergency departments in Shandong Province, China. The primary endpoint was 30-day major adverse cardiac events (MACEs). Overlap propensity score weighting was used to address potential confounding. A total of 8046 patients were analysed (42.8% female). Overlap-weighted analysis showed no significant association of female sex with 30-day MACEs (odds ratio, 0.91; 95% CI 0.75 to 1.11; P = 0.363). Secondary analyses found that women were less likely to be identified as high risk at first presentation (odds ratio, 0.86; 95% CI 0.78 to 0.94; P < 0.001). In the emergency department, women were less likely to undergo antiplatelet therapy (odds ratio, 0.87; 95% CI 0.79 to 0.96; P = 0.004) or coronary angiography (odds ratio, 0.78; 95% CI, 0.69 to 0.88; P < 0.001). Women had a longer length of stay in the emergency department and were less likely to be admitted to a ward at disposition. These sex differences existed only in the non-ST-elevation subgroup and were independent of risk stratification. Women with non-ST-elevation chest pain in China received suboptimal treatment in the emergency department. However, their clinical outcomes were not significantly different from those of men. Further studies are needed to determine the causes and impacts of these sex differences.

[Trauma assessment and first aid in the confined spaces after major natural disasters].

Major natural disasters seriously threaten human life and health. After earthquakes and other catastrophes, survivors are often trapped in the confined spaces caused by the collapse of ground and buildings, with relative separation from the outside world, restricted access, complex environment, and oncoming or ongoing unsafety, leading to the rescue extremely difficult. In order to save lives and improve the outcome more efficiently in the confined spaces after natural disasters, it is very important to standardize and reasonably apply the trauma assessment and first aid workflow. This study focuses on trauma assessment and first aid. From the aspects of trauma assessment, vital signs stabilization, hemostasis and bandaging, post-trauma anti-infection, and the transportation of patients, a trauma first aid work process suitable for a small space of a major natural disaster is formed, It is helpful to realize the immediate and efficient treatment of trauma in the confined spaces after natural catastrophes, to reduce the rate of death and disability and improve the outcome of patients.

[Research progress of in-hospital mortality risk model in patients with acute myocardial infarction].

The incidence of in-hospital death in acute myocardial infarction (AMI) is high, which seriously threatens the life and health of patients. At present, many countries and regions have established a variety of objective assessment models for predicting the in-hospital mortality of patients with AMI, providing important decision-making support for patients with different risk levels when formulating treatment plans. With the rise of artificial intelligence, many new modeling methods also show certain advantages over the traditional models. This article systematically introduces the commonly used and newly constructed risk prediction models for in-hospital mortality of AMI, in order to provide help for medical staff to assist decision-making in clinical practice, and provide reference for the establishment of a safe and more effective risk prediction model in the future.

Macrophage ALDH2 (Aldehyde Dehydrogenase 2) Stabilizing Rac2 Is Required for Efferocytosis Internalization and Reduction of Atherosclerosis Development.

BACKGROUND: Clinical studies show that the most common single-point mutation in humans, ALDH2 (aldehyde dehydrogenase 2) rs671 mutation, is a risk factor for the development and poor prognosis of atherosclerotic cardiovascular diseases, but the underlying mechanism remains unclear. Apoptotic cells are phagocytosed and eliminated by macrophage efferocytosis during atherosclerosis, and enhancement of arterial macrophage efferocytosis reduces atherosclerosis development. METHODS: Plaque areas, necrotic core size, apoptosis, and efferocytosis in aortic lesions were investigated in APOE-/- mice with bone marrow transplanted from APOE-/-ALDH2-/- and APOE-/- mice. RNA-seq, proteomics, and immunoprecipitation experiments were used to screen and validate signaling pathways affected by ALDH2. Efferocytosis and protein levels were verified in human macrophages from wild-type and rs671 mutation populations. RESULTS: We found that transplanting bone marrow from APOE-/-ALDH2-/- to APOE-/- mice significantly increased atherosclerosis plaques compared with transplanting bone marrow from APOE-/- to APOE-/- mice. In addition to defective efferocytosis in plaques of APOE-/- mice bone marrow transplanted from APOE-/-ALDH2-/- mice in vivo, macrophages from ALDH2-/- mice also showed significantly impaired efferocytotic activity in vitro. Subsequent RNA-seq, proteomics, and immunoprecipitation experiments showed that wild-type ALDH2 directly interacted with Rac2 and attenuated its degradation due to decreasing the K48-linked polyubiquitination of lysine 123 in Rac2, whereas the rs671 mutant markedly destabilized Rac2. Furthermore, Rac2 played a more crucial role than other Rho GTPases in the internalization process in which Rac2 was up-regulated, activated, and clustered into dots. Overexpression of wild-type ALDH2 in ALDH2-/- macrophages, rather than the rs671 mutant, rescued Rac2 degradation and defective efferocytosis. More importantly, ALDH2 rs671 in human macrophages dampened the apoptotic cells induced upregulation of Rac2 and subsequent efferocytosis. CONCLUSIONS: Our study has uncovered a pivotal role of the ALDH2-Rac2 axis in mediating efferocytosis during atherosclerosis, highlighting a potential therapeutic strategy in cardiovascular diseases, especially for ALDH2 rs671 mutation carriers.

Comparison of Safety and Efficacy Between Clopidogrel and Ticagrelor in Elderly Patients With Acute Coronary Syndrome: A Systematic Review and Meta-Analysis.

Background: Dual antiplatelet therapy combining aspirin with a P2Y12 adenosine diphosphate receptor inhibitor is a therapeutic mainstay for acute coronary syndrome (ACS). However, the optimal choice of P2Y12 adenosine diphosphate receptor inhibitor in elderly (aged ≥65 years) patients remains controversial. We conducted a meta-analysis to compare the efficacy and safety of ticagrelor and clopidogrel in elderly patients with ACS. Methods: We comprehensively searched in Web of Science, EMBASE, PubMed, and Cochrane databases through 29th March, 2021 for eligible randomized controlled trials (RCTs) comparing the efficacy and safety of ticagrelor or clopidogrel plus aspirin in elderly patients with ACS. Four studies were included in the final analysis. A fixed effects model or random effects model was applied to analyze risk ratios (RRs) and hazard ratios (HRs) across studies, and I2 to assess heterogeneity. Results: A total number of 4429 elderly patients with ACS were included in this analysis, of whom 2170 (49.0%) patients received aspirin plus ticagrelor and 2259 (51.0%) received aspirin plus clopidogrel. The ticagrelor group showed a significant advantage over the clopidogrel group concerning all-cause mortality (HR 0.78, 95% CI 0.63-0.96, I2 = 0%; RR 0.79, 95% CI 0.66-0.95, I2 = 0%) and cardiovascular death (HR 0.71, 95% CI 0.56-0.91, I2 = 0%; RR 0.76, 95% CI 0.62-0.94, I2 = 5%) but owned a higher risk of PLATO major or minor bleeding (HR 1.46, 95% CI 1.13-1.89, I2 = 0%; RR 1.40, 95% CI 1.11-1.76, I2 = 0%). Both the groups showed no significant difference regarding major adverse cardiovascular events (MACEs) (HR 1.06, 95% CI 0.68-1.65, I2 = 77%; RR 1.04, 95% CI 0.69-1.58, I2 = 77%). Conclusion: For elderly ACS patients, aspirin plus ticagrelor reduces cardiovascular death and all-cause mortality but increases the risk of bleeding. Herein, aspirin plus ticagrelor may extend lifetime for elderly ACS patients compared with aspirin plus clopidogrel. The optimal DAPT for elderly ACS patients may be a valuable direction for future research studies.

Development and Validation of a Simple-to-Use Nomogram for Predicting In-Hospital Mortality in Patients With Acute Heart Failure Undergoing Continuous Renal Replacement Therapy.

Background: Patients with acute heart failure (AHF) who require continuous renal replacement therapy (CRRT) have a high risk of in-hospital mortality. It is clinically important to screen high-risk patients using a model or scoring system. This study aimed to develop and validate a simple-to-use nomogram consisting of independent prognostic variables for the prediction of in-hospital mortality in patients with AHF undergoing CRRT. Methods: We collected clinical data for 121 patients with a diagnosis of AHF who underwent CRRT in an AHF unit between September 2011 and August 2020 and from 105 patients in the medical information mart for intensive care III (MIMIC-III) database. The nomogram model was created using a visual processing logistic regression model and verified using the standard method. Results: Patient age, days after admission, lactic acid level, blood glucose concentration, and diastolic blood pressure were the significant prognostic factors in the logistic regression analyses and were included in our model (named D-GLAD) as predictors. The resulting model containing the above-mentioned five factors had good discrimination ability in both the training group (C-index, 0.829) and the validation group (C-index, 0.740). The calibration and clinical effectiveness showed the nomogram to be accurate for the prediction of in-hospital mortality in both the training and validation cohort when compared with other models. The in-hospital mortality rates in the low-risk, moderate-risk, and high-risk groups were 14.46, 40.74, and 71.91%, respectively. Conclusion: The nomogram allowed the optimal prediction of in-hospital mortality in adults with AHF undergoing CRRT. Using this simple-to-use model, the in-hospital mortality risk can be determined for an individual patient and could be useful for the early identification of high-risk patients. An online version of the D-GLAD model can be accessed at https://ahfcrrt-d-glad.shinyapps.io/DynNomapp/. Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT0751838.

Aldehyde dehydrogenase 2 protects against acute kidney injury by regulating autophagy via the Beclin-1 pathway.

The mitochondrial enzyme aldehyde dehydrogenase 2 (ALDH2) catalyzes the detoxification of acetaldehyde and endogenous lipid aldehydes. Approximately 40% of East Asians, accounting for 8% of the human population, carry the E504K mutation in ALDH2 that leads to accumulation of toxic reactive aldehydes and increases the risk for cardiovascular disease, cancer, and Alzheimer disease, among others. However, the role of ALDH2 in acute kidney injury (AKI) remains poorly defined and is therefore the subject of the present study using various cellular and organismal sources. In murine models, in which AKI was induced by either the contrast agent iohexol or renal ischemia/reperfusion, KO, activation/overexpression of ALDH2 were associated with increased and decreased renal injury, respectively. In murine renal tubular epithelial cells (RTECs), ALDH2 upregulated Beclin-1 expression, promoted autophagy activation, and eliminated ROS. In vivo and in vitro, both 3-MA and Beclin-1 siRNAs inhibited autophagy and abolished ALDH2-mediated renoprotection. In mice with iohexol-induced AKI, ALDH2 knockdown in RTECs using AAV-shRNA impaired autophagy activation and aggravated renal injury. In human renal proximal tubular epithelial HK-2 cells exposed to iohexol, ALDH2 activation potentiated autophagy and attenuated apoptosis. In mice with AKI induced by renal ischemia/reperfusion, ALDH2 overexpression or pretreatment regulated autophagy mitigating apoptosis of RTECs and renal injury. In summary, our data collectively substantiate a critical role of ALDH2 in AKI via autophagy activation involving the Beclin-1 pathway.

Five-year outcomes comparing percutaneous coronary intervention with drug-eluting stents versus coronary artery bypass grafting in patients with left main coronary artery disease: A systematic review and meta-analysis.

BACKGROUND AND AIMS: In patients with left main coronary artery disease (LMCAD), long-term outcomes after percutaneous coronary intervention (PCI) with drug-eluting stents (DES) compared with coronary artery bypass grafting (CABG) remain controversial. We conducted a meta-analysis to compare the efficacy and safety of PCI with DES and CABG in LMCAD patients. METHODS: We comprehensively searched in Web of Science, EMBASE, PubMed, and Cochrane databases for eligible randomised controlled trials (RCTs) comparing the 5-year clinical outcomes between PCI with DES and CABG in LMCAD patients. Random-effect models were applied to analyse risk ratios (RRs) and hazard ratios (HRs) across studies, and I2 to assess heterogeneity. RESULTS: We screened 4 RCTs including 4394 patients distributed randomly into PCI (n = 2197) and CABG (n = 2197) groups. In comparison to CABG, PCI showed non-inferiority concerning a composite of death, myocardial infarction, and stroke (HR 1.22, 95% confident interval [CI] 0.84-1.75), death (HR 1.06, 95% CI 0.81-1.40) and stroke (HR 0.80, 95% CI 0.42-1.53). Regarding major adverse cardiac or cerebrovascular events (MACCE) rate, both strategies show clinical equipoise in patients with a low-to-intermediate Synergy Between PCI with TAXUS and Cardiac Surgery (SYNTAX) score (HR 1.20, 95% CI 0.85-1.70), while CABG had an advantage over PCI in those with a high SYNTAX score (HR 1.64, 95% CI 1.20-2.24). CONCLUSIONS: CABG showed advantage over PCI with DES for LMCAD patients in MACCE. PCI and CABG showed equivalent 5-year clinical risk of a composite of all-cause mortality, myocardial infarction, and stroke, but the former had higher risk of repeat revascularization.

Prevention of aortic dissection and aneurysm via an ALDH2-mediated switch in vascular smooth muscle cell phenotype.

AIMS: Aortic aneurysm/dissection (AAD) is a life-threatening disorder lacking effective pharmacotherapeutic remedies. Aldehyde dehydrogenase 2 (ALDH2) polymorphism is tied with various risk factors for AAD including hypertension, atherosclerosis, and hypercholesterolaemia although direct correlation between the two remains elusive. METHODS AND RESULTS: Two independent case-control studies were conducted involving 307 AAD patients and 399 healthy controls in two geographically distinct areas in China. Our data revealed that subjects carrying mutant ALDH2 gene possessed a ∼50% reduced risk of AAD compared with wild-type (WT) alleles. Using 3-aminopropionitrile fumarate (BAPN)- and angiotensin II (Ang II)-induced AAD animal models, inhibition of ALDH2 was found to retard development of AAD. Mechanistically, ALDH2 inhibition ablated pathological vascular smooth muscle cell (VSMC) phenotypical switch through interaction with myocardin, a determinant of VSMC contractile phenotype. Using microarray and bioinformatics analyses, ALDH2 deficiency was found to down-regulate miR-31-5p, which further altered myocardin mRNA level. Gain-of-function and loss-of-function studies verified that miR-31-5p significantly repressed myocardin level and aggravated pathological VSMC phenotypical switch and AAD, an effect that was blunted by ALDH2 inhibition. We next noted that ALDH2 deficiency increased Max expression and decreased miR-31-5p level. Moreover, ALDH2 mutation or inhibition down-regulated levels of miR-31-5p while promoting myocardin downstream contractile genes in the face of Ang II in primary human VSMCs. CONCLUSIONS: ALDH2 deficiency is associated with a lower risk of AAD in patients and mice, possibly via suppressing VSMC phenotypical switch in a miR-31-5p-myocardin-dependent manner. These findings favour a role for ALDH2 and miR-31-5p as novel targets for AAD therapy.

[Early prevention progress of contrast induced nephropathy].

OBJECTIVE: Contrast induced nephropathy (CIN) is acute renal injury following administration of contrast media during angiographic or other medical procedures, which represents as the third cause of hospital-acquired renal failure. CIN is associated with prolonged hospital stay, increased health-care costs, and undesirable clinical outcome. The risk of CIN includes advanced age and diabetes mellitus. With the rapid development of iconography and the wide application of interventional techniques, the patients with CIN are increasing. The preventive measures of CIN include hydration, using appropriate contrast media, stopping nephrotoxic drugs, ischemic preconditioning, renal replacement therapy, and using appropriate drugs. In this paper, the current status and early prevention progress of CIN will be reviewed from three aspects of the high-risk factors, pathogenesis and prevention, aiming to provide guidance for the early prevention of CIN and explore new research directions.

Omission of aspirin in patients taking oral anticoagulation after percutaneous coronary intervention: a systematic review and meta-analysis.

BACKGROUND: There is no consensus on optimal antiplatelet and anticoagulation therapy after coronary stenting. METHODS: We identified randomized controlled trials (RCTs) published in PubMed, Cochrane Library, and Embase using the following keywords: 'antiplatelet', 'dual therapy', 'triple therapy', 'antithrombosis', 'indication for anticoagulation', 'percutaneous coronary intervention', and 'RCTs'. Primary safety end points were relative bleeding events, and secondary efficacy end points were major adverse cardiovascular events including stent thrombosis, death, myocardial infarction, and stroke. RESULTS: We identified three RCTs including 5387 patients, of whom 2719 (50.5%) received dual therapy (DT) and 2668 (49.5%) received triple therapy. Relative to triple therapy, DT was associated with lower Thrombolysis in Myocardial Infarction major bleeding [risk ratio (RR): 0.58; 95% confidence interval (CI): 0.42-0.82], Thrombolysis in Myocardial Infarction minor bleeding (RR: 0.46; 95% CI: 0.34-0.62), and clinical bleeding events (RR: 0.61; 95% CI: 0.47-0.81). There was no significant difference for the secondary efficacy end point. In subgroup analyses, results were similar by sex, bleeding risk, and stent type; however, DT appeared suitable for patients aged less than 75 years but not more than or equal to 75 years, implying that there may be no ideal therapy for patients older than 75 years to balance the risk of ischemia and bleeding at the same time. CONCLUSION: Among patients with an indication for oral anticoagulation after percutaneous coronary intervention, DT appears to be the optimal strategy.

Protective effects of ethyl acetate extracts of Rimulus Cinnamon on systemic inflammation and lung injury in endotoxin-poisoned mice.

Rimulus cinnamon is the dried twig of Cinnamomum cassia Presl. It is widely used in China for the treatment of inflammatory processes, amenorrhea, and other diseases. We aimed to study the protective effects of ethyl acetate extracts of R. cinnamon (EAE) on systemic inflammation and lung injury in endotoxin-poisoned mice. EAE was administered 5 d prior to lipopolysaccharide (LPS) challenge with 15 mg/kg LPS. The administration of EAE increased the levels of interferon-γ (IFN-γ) and decreased the levels of interleukin-18 (IL-18) and tumor necrosis factor-α (TNF-α) in the serum. Additionally, EAE relieved the pathological changes in the tissues of the lungs and spleen, and significantly reduced the number of neutrophils in the lung tissues. In addition, treatment with EAE decreased the mRNA expression of the NLR family, pyrin domain-containing protein 3 (NLRP3), caspase-1, and interleukin-1ß (IL-1ß) in the lungs, as well as the expression of NLRP3, caspase-1 (p20), and pro-IL-1ß proteins. These results demonstrated the promising anti-inflammatory effects of EAE in endotoxin-poisoned mice. Furthermore, EAE could alleviate the lung injury of endotoxin-poisoned mice by antagonizing the activation of the NLRP3 inflammasome.

Protective effects of essential oils from Rimulus cinnamon on endotoxin poisoning mice.

The essential oils from Rimulus cinnamon (EORC) have anti-inflammation activities, but the effects of EORC on endotoxin poisoning mice remain to be explored, the mechanism is still unclear. This study was designed to investigate the protective effects and mechanism of EORC on lipopolysaccharide (LPS)-induced endotoxin poisoning mice. Pre-treatment with EORC decreased the production of pro-inflammatory cytokines (Interleukin-1ß, Interleukin-18, Interleukin-5, and Interferon-γ) and chemokines (Monocyte chemotactic protein-1, Macrophage colony-stimulating factor, and Macrophage inflammatory protein-1ß) in serum of endotoxin poisoning mice. The histopathological study showed that the lung injury was improved and EORC decreased the numbers of neutrophils and Nitric oxide (NO) levels in lung. EORC could reduce the mRNA expression of NLR family, pyrin domain-containing 3 (NLRP3), Interleukin (IL)-1ß, and nitric oxide synthase (iNOS). In addition, EORC decreased the protein expression of NLRP3, Caspase-1 (p20), Pro-IL-1ß, and purinergic P2 × 7 receptor (P2 × 7R) in the lung tissues. The results above indicated that the EORC may have protective effects on LPS-induced endotoxin poisoning mice via inhibiting the activation of P2 × 7R/NLRP3 inflammasome.

Protective effect of cinnamic acid in endotoxin-poisoned mice.

In this work, we aimed to evaluate the protective effect of cinnamic acid (CD) on lipopolysaccharide (LPS; Escherichia coli 055:B5)-induced endotoxin-poisoned mice and clarify the underlying mechanisms. The mice were administrated CD 5 d before 15 mg/kg LPS challenge. 12 hr later, thymus was separated for determination of thymus indexes. Lung and spleen tissues were collected for histologic examination and the wet/dry weight ratio of lung was calculated, and serum was acquired for tumor necrosis factor-α (TNF-α), interleukin (IL)-18, and IL-1ß measurement. Moreover, the expression of NOD-like receptor (NLR) family, pyrin domain-containing 3 (NLRP3) inflammasome was determined in lung. CD increased the thymus indexes and decreased lung wet/dry weight ratio. In addition, CD improved the lung and spleen histopathological changes induced by LPS and decreased the number of neutrophils in lung tissues. CD also inhibited the pro-inflammatory cytokines (TNF-α, IL-18, and IL-1ß) production in serum. Furthermore, CD suppressed the LPS-induced NLRP3, Caspase-1, and IL-1ß mRNA expression in lung, as well as the expression of NLRP3 and Caspase-1 (p20) protein. CD may have protective effects in endotoxin-poisoned mice via inhibiting the activation of NLRP3 inflammasome, and can be considered as a potential therapeutic candidate for diseases involved in endotoxin poisoning such as sepsis.

Inhibition of NLRP3 inflammasome: a new protective mechanism of cinnamaldehyde in endotoxin poisoning of mice.

CONTEXT: Cinnamaldehyde (CA) has a protective effect in endotoxin poisoning of mice, but there is no direct evidence for the protective effect of CA through inhibition of NLRP3 inflammasome activation in endotoxin poisoning of mice. OBJECTIVE: We aimed to investigate the protective mechanism of CA in endotoxin poisoned mice through NLRP3 inflammasome. MATERIALS AND METHODS: First, we evaluated the anti-inflammatory effect of CA in phorbol-12-myristate acetate-differentiated THP-1 cells through the NLRP3 inflammasome. Second, in a mouse model of lipopolysaccharide (LPS)-induced endotoxin poisoning, CA was administrated for 5 d (once a day) before the 15 mg/kg LPS challenge. Then, the levels of IL-1ß in serum were measured, and the effect of CA on the NLRP3 inflammasome activation and the expression of cathepsin B and P2X7R proteins in lung were explored. RESULTS: In vitro, CA decreased the levels of p20, pro-IL-1ß and IL-1ß in cell culture supernatants, as well as the expression of NLRP3 and IL-1ß mRNA in cells. In vivo, CA decreased IL-1ß production in serum. Furthermore, CA suppressed LPS-induced NLRP3, p20, Pro-IL-1ß, P2X7 receptor (P2X7R) and cathepsin B protein expression in lung, as well as the expression of NLRP3 and IL-1ß mRNA. CONCLUSIONS: CA has a protective effect in the endotoxin poisoned mice through the inhibition of NLRP3 inflammasome activation. Furthermore, CA suppresses the NLRP3 inflammasome activation by inhibiting the expression of cathepsin B and P2X7R protein expression. CA can be considered as a potential therapeutic candidate for diseases involved in endotoxin poisoning such as sepsis.

Protective effect of cinnamicaldehyde in endotoxin poisoning mice.

CONTEXT: Several pharmacological studies have shown that cinnamicaldehyde (CA) has anti-inflammatory and anti-tumor effects, but no data show the effects of CA on the endotoxin poisoning. OBJECTIVE: In this work, the protective effect of CA in LPS-induced endotoxin poisoning mice was investigated. MATERIALS AND METHODS: Mice were randomly divided into normal, LPS, LPS +5 mg/kg dexamethasone (DEX), LPS +0.132 g/kg CA, and LPS +0.264 g/kg CA group. Pretreated with CA (0.132 and 0.264 g/kg/day, respectively) for 5 consecutive days before LPS injection. Except the normal group, the other animals were intraperitoneally injected with LPS (15 mg/kg). RESULTS: Twelve hours after LPS injection, CA significantly reduced the production of pro-inflammatory cytokines (interleukin-18, interleukin-1ß, and interleukin-5) and chemokines (macrophage colony stimulating factor, macrophage inflammatory protein-1ß) in serum. In addition, the histopathological study indicated that CA attenuates lung injury induced by LPS. Moreover, the numbers of neutrophils were significant decreased and the NF-κB (p65) mRNA level was reduced in lung after treated with CA. CONCLUSION: The present data suggest that cinnamicaldehyde can be considered as potential therapeutic candidates for the endotoxin-poisoning-related diseases such as sepsis via its anti-inflammation effects.

[Protective effects of Schizonepeta volatile oil on endotoxin poisoning induced by lipopolysaccharide in mice].

In order to study the protective effects of Schizonepeta volatile oil (Sto）on endotoxin poisoning mice, and the relatively content of each chemical osubstance in Schizonepeta volatile oil was measured using GC-MS. The mare C57BL/6J mice were randomly divided into five groups including the normal group, model group, dexamethasone group (5 mg•kg⁻¹), and Sto (0.226 and 0.452 g•kg⁻¹, respectively) groups. The dexamethasone group was given the drugs once time by intraperitoneal injection on the 5th day, while the other mice were given drugs by oral administration once a day for 5 days. Then, the normal group was injected with the saline and the other groups were injected LPS (15 mg•kg-1) after 30 minutes of the last administration. After LPS injection twelve hours, the blood, serum, and lung tissue of mice were collected. The IL-18, IL-1ß, IL-5, TNF-α, MCP-1, MIP-1ß, M-CSF, and GM-CSF were measured in serum by ELISA and Luminex Magpix. The white cell (WBC) and platelet (PLT) in blood were counted and lung, spleen, and thymus index were calculated. The lung histopathology was performed at the same time. The GC-MS results showed that the relative content of menthone and pulegone are 46.67% and 33.92%, respectively. The Sto (0.452 and 0.226 g•kg⁻¹, respectively) reduced the levels of IL-1ß, IL-5, TNF-α, MCP-1, MIP-1ß, and M-CSF in serum (P<0.01 or P<0.05). The 0.452 g•kg⁻¹ Sto also reduced the levels of IL-18 and GM-CSF in the serum (P<0.01 or P<0.05). And the 0.226 g•kg⁻¹ Sto showed good anti-inflammatory effects by reducing neutrophil infiltration in the lung tissue. But the Sto had no effect on the increasing of WBC, spleen and lung index as well as decreasing of PLT and thymus index. The results showed that Sto has a protective effect in LPS-induced exdotoxin poisoning mice, its mechanism is related to inhibit the release of varies of inflammatory cytokines and reduce the inflammation reaction.