This study aimed to investigate the anti-inflammatory and antioxidant effects of atractylon on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Changes in lung function parameters were measured in mice after intraperitoneal administration of atractylon. Pathological changes in lung tissue were observed by H&E staining, and the degree of pulmonary edema was assessed by the lung wet/dry weight ratio (W/D). Kit assays were used to detect changes in oxidative stress markers in mouse serum and the protein concentration in bronchoalveolar lavage fluid (BALF). ELISA was employed to measure the expression levels of inflammatory cytokines in BALF and serum. Western blot was used to detect the expression levels of proteins related to the cGAS-STING pathway and vascular cell adhesion molecule-1 (VCAM-1) in lung tissue. Results showed that, compared to the ALI model group, mice in the low-dose and high-dose atractylon groups exhibited significant improvement in lung function parameters, alleviated pulmonary edema, and reduced inflammatory cell infiltration in lung tissue. Protein content and inflammatory cytokine levels in serum and BALF were decreased, while serum oxidative stress indicators were improved. Western blot results further indicated that atractylon could regulate the cGAS-STING pathway, blocking the generation of inflammatory signals, and simultaneously inhibit VCAM-1 expression, thereby reducing pulmonary vascular injury. The results suggest that atractylon may alleviate LPS-induced ALI by modulating the cGAS-STING signaling pathway, reducing the expression of pro-inflammatory cytokines and the production of pro-inflammatory mediators, and improving vascular endothelial injury. This study provides a new potential target and theoretical basis for the treatment of ALI, as well as a potential drug candidate for ALI therapy.

Objective To investigate the possible mechanism of ferroptosis induced by lipocalin2(LCN2)and microglial po-larization in intracerebral hemorrhage(ICH).Methods Forty SD rats were divided into sham operation group,ICH group,LCN2 low expression group and Liproxstatin-1 group,with 10 rats in each group.The morphological structure of the brain was observed and recorded,and the cranial nerve function(NIHSS)score was performed.Immunofluorescence staining was used to detect the expression of microglia marker protein(Iba1),and M1 and M2 microglia marker proteins(CD68 and CD206)in brain tissue.Western blot was used to detect the protein levels of LCN2,ferroptosis marker proteins[solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4)]in brain tissue.The contents of ferrous ion(Fe2+)and malondialdehyde(MDA)in brain tissue were detected by ELISA kits.Results Compared with the sham operation group,the expression of LCN2 protein,the intracerebral hemorrhage,the NIHSS score increased(all P＜0.05),and the expression of CD68 and CD206 in the microglia increased,the expression of ferroptosis-related proteins(SLC7A11 and GPX4)decreased,and the content of Fe2+and MDA increased in the brain tissue of the ICH group(all P＜0.05).Compared with the ICH group,the expression of LCN2 pro-tein,the intracerebral hemorrhage,the NIHSS score and the expression of CD68 in microglia significantly decreased,and the ex-pression of CD206 significantly increased,the expression of SLC7A11 and GPX4 increased,the contents of Fe2+and MDA de-creased in the brain tissue of the LCN2 low expression group(all P＜0.05).The expression of CD68 in brain tissue of Liprox-statin-1 group was significantly decreased,and the expression of CD206 was significantly increased as compared with ICH group(P＜0.05).Conclusion Down-regulation of LCN2 can promote microglial cell polarization by inhibiting ferroptosis,and im-prove nerve function injury in ICH rats.

Objective To investigate the possible mechanism of ferroptosis induced by lipocalin2(LCN2)and microglial po-larization in intracerebral hemorrhage(ICH).Methods Forty SD rats were divided into sham operation group,ICH group,LCN2 low expression group and Liproxstatin-1 group,with 10 rats in each group.The morphological structure of the brain was observed and recorded,and the cranial nerve function(NIHSS)score was performed.Immunofluorescence staining was used to detect the expression of microglia marker protein(Iba1),and M1 and M2 microglia marker proteins(CD68 and CD206)in brain tissue.Western blot was used to detect the protein levels of LCN2,ferroptosis marker proteins[solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4)]in brain tissue.The contents of ferrous ion(Fe2+)and malondialdehyde(MDA)in brain tissue were detected by ELISA kits.Results Compared with the sham operation group,the expression of LCN2 protein,the intracerebral hemorrhage,the NIHSS score increased(all P＜0.05),and the expression of CD68 and CD206 in the microglia increased,the expression of ferroptosis-related proteins(SLC7A11 and GPX4)decreased,and the content of Fe2+and MDA increased in the brain tissue of the ICH group(all P＜0.05).Compared with the ICH group,the expression of LCN2 pro-tein,the intracerebral hemorrhage,the NIHSS score and the expression of CD68 in microglia significantly decreased,and the ex-pression of CD206 significantly increased,the expression of SLC7A11 and GPX4 increased,the contents of Fe2+and MDA de-creased in the brain tissue of the LCN2 low expression group(all P＜0.05).The expression of CD68 in brain tissue of Liprox-statin-1 group was significantly decreased,and the expression of CD206 was significantly increased as compared with ICH group(P＜0.05).Conclusion Down-regulation of LCN2 can promote microglial cell polarization by inhibiting ferroptosis,and im-prove nerve function injury in ICH rats.

AIM:This study investigates the apoptotic and autophagic effects of atractylodin on lung cancer cells,elucidating the underlying molecular mechanisms.METHODS:Non-small cell lung cancer(NSCLC)A549 and H460 cells,in addition to non-cancerous HBE cells,were cultured in vitro.The effects of atractylodin at various concen-trations on cell viability were assessed using CCK-8 assay.Apoptotic effects were evaluated through Hoechst staining and flow cytometry,while Western blot analysis was performed to detect changes in protein expressions associated with apopto-sis and autophagy,including P62,beclin-1,microtubule-associated protein 1 light chain 3(LC3),Kelch-like epichloro-hydrin(ECH)-associated protein-1(Keap-1),nuclear factor E2-related factor 2(Nrf2),heme oxygenase-1(HO-1),and NAD(P)H:quinone oxidoreductase 1(NQO1).Autophagic flux was further analyzed using acridine orange(AO)stain-ing,and immunofluorescence for LC3 and Nrf2.Additionally,autophagy inhibition experiments were conducted using chloroquine(CQ),followed by analyses of autophagy and apoptosis.Reactive oxygen species(ROS)levels were quanti-fied using DCFH-DA.RESULTS:Treatment with atractylodin significantly reduced the viability of A549 and H460 lung cancer cells,promoting apoptosis and inducing autophagy.This was evidenced by an increase in acidic autophagic vesi-cles,upregulation of LC3 and beclin-1,and downregulation of P62.Inhibition of autophagy by chloroquine reversed atrac-tylodin-induced apoptosis.Moreover,atractylodin heightened ROS production,inhibited Keap-1,and stimulated the ex-pression of Nrf2,HO-1 and NQO1.CONCLUSION:Atractylodin effectively inhibits the proliferation of lung cancer cells by inducing apoptosis and autophagy.These effects are mediated through the modulation of the ROS/Nrf2/HO-1 sig-naling pathway,underscoring its potential as a therapeutic agent in lung cancer treatment.

Objective To investigate the risk factors associated with post traumatic cerebral infarction (PTCI) after craniotomy hematoma evacuation for severe traumatic brain injury (sTBI) so as to provide clinical reference for the early prevention of postoperative PTCI.Methods A retrospective case control study was conducted to analyze the clinical data of 558 sTBI patients who received craniotomy hematoma evacuation admitted to Changsha Hospital of Traditional Chinese Medicine from October 2006 to June 2016.There were 340 males and 218 females,aged 15-71 years,with an average of 47.8 years.Among them,75 patients were at the age of less than 30 years,315 were at 30-50 years,and 168 were above 50 years.According to the Glasgow coma score (GCS),there were 127 patients with 3-4 points,124 with 5-6 points,and 307 with 7-8 points.The patients were divided into PTCI group (51 patients)and non-PTCI group (507 patients).The related indicators of the two groups of patients after admission were collected,including gender,age,injury cause,GCS,skull base fracture,traumatic subarachnoid hemorrhage (tSAH),cerebral hernia,hypotension,the time from injury to craniotomy,and whether decompressive craniectomy was performed.Univariate analysis was first performed for these factors,followed by multivariate logistic regression analysis.Results There were no significant differences in gender,age,injury cause,skull base fracture,and decompressive craniectomy between PTCI group and control group (P ＞ 0.05).In the PTCI group,there were 29 patients with GCS of 3-4 points,17 with 5-6 points,and five with 7-8 points;there were 48 patients with tSAH,37 patients with cerebral hernia,and 18 patients with hypotension.In terms of the time from injury to craniotomy,it took ＜ 3 hours in 30 patients,3-6 hours in 12,6-12 hours in five,and ＞ 12 hours in four.In the non-PTCI group,there were 98 patients with GCS of 3-4 points,107 with 5-6 points,and 302 with 7-8 points.There were 34 patients with tSAH,117 with cerebral hernia,and 35 with hypotension.In terms of the time from injury to craniotomy,it took ＜3 hours in 294 patients,3-6 hours in 130,6-12 hours in 68,and ＞ 12 hours in 15.The differences between the two groups were statistically significant (P ＜ 0.05).Multivariate logistic regression analysis indicated that GCS of 3-6 points,tSAH,cerebral hernia,time from injury to craniotomy,and hypotension were significantly associated with PTCI after operation for sTBI (P ＜ 0.01).Conclusions GCS of 3-6 points,tSAH,cerebral hernia,duration from injury to craniotomy,and hypotension time ＞ 3 hours are the high risk factors of PTCI in sTBI patients after craniotomy.For patients with these high risk factors,craniotomy should be performed in time,and the perioperative blood pressure and intracranial pressure stability should be maintained so as to relieve vasospasm.