Objective:To explore the correlation between systemic inflammatory response index (SIRI) and clinical outcome of patients with massive cerebral infarction (MCI) after craniotomy and decompression.Methods:The clinical data of 50 MCI patients who were treated in the Affiliated Hospital of Qingdao University from January 2016 to December 2020 and underwent craniotomy and decompression were retrospectively analyzed. The measurement data of normal distribution were expressed as xˉ± s, and the measurement data of non normal distribution were expressed as M( Q1, Q3). T-test or rank sum test was used for comparison between the two groups. Multivariate Logistic regression was used to analyze the relationship between SIRI and prognosis of MCI patients and establish a prediction model. The predictive value and optimal cutoff value of SIRI were analyzed by receiver operating characteristic curve (ROC). Results:Among the 50 MCI patients who underwent craniotomy and decompression, 12 (24%, 12/50) had a good prognosis; In the poor prognosis group, 38 cases (76%, 12/50), of which 9 cases (18%, 9/50) died during hospitalization. The age of patients in the good prognosis group and the poor prognosis group ((54±11) years and (63±9) years; t=2.72, P=0.015), body mass index (BMI): ((23.91±2.64) kg/m 2 and (26.72±3.28) kg/m 2, t=3.01, P=0.006)), neutrophil count (7.08 (5.12, 7.38))×10 9/L and 10.59 (8.91,14.64)×10 9/L, Z=5.72, P<0.001), white blood cell count ((9.09±2.80)×10 9/L and (13.20±3.49) ×10 9/L; t=4.16, P<0.001), SIRI (2.49(1.78, 4.75) and 8.34(5.17, 13.61); Z=3.84, P<0.001), Glasgow Coma Score (12(9,14) and 8(6,10); Z=3.36, P=0.002) and lymphocyte count (1.58(0.91, 1.91)×10 9/L and 0.77(0.59,1.02) ×10 9/L; Z=3.30, P=0.001).The difference between the two groups was statistically significant. The prognosis of patients with dominant hemisphere infarction was worse than that of patients with non-dominant hemisphere infarction (22 cases (91.67%, 22/24) vs. 16 cases (61.54%, 16/26); χ 2=6.21, P=0.013). The ICU stay in the good prognosis group was significantly shorter than that in the poor prognosis group (2 (1, 5) days vs. 8 (3, 19) days; Z=2.78, P=0.005). Multivariate Logistic regression analysis showed that SIRI and GCS were correlated with clinical prognosis: SIRI ( OR: 2.378; 95% CI: 1.131-5.003; P=0.022); GCS at admission ( OR: 0.548; 95% CI: 0.307-0.980; P=0.043). The ROC curve analysis of SIRI prediction of poor prognosis: Area under the curve (AUC): 0.871, (95% CI: 0.765-0.976, P<0.001), sensitivity was 78.9%, specificity was 88.3%, and the optimal cut-off value was 4.96. The sensitivity, specificity and AUC of GCS for predicting poor prognosis after MCI craniotomy decompression were 89.5%, 58.3% and 0.791 (95% CI: 0.638~0.943, P=0.003), and the best truncation value was 11.5. Conclusion:SIRI was an effective predictor of clinical outcome for MCI patients underwent Craniotomy for decompression, and SIRI value greater than 4.96 indicates adverse clinical outcome.

ObjectiveTo investigate the effect of linalool against acute liver injury induced by aflatoxin B₁（AFB₁） in rats and explore its protective mechanism. MethodTwenty male SPF SD rats were randomly divided into three groups： Control （n=6）， AFB₁ （n=7）， and linalool （n=7） groups. Linalool solution （200 mg·kg^-1） was administered preventatively for 14 days， while the control and AFB₁ groups intragastrically received an equivalent volume of double distilled water. After preventative administration of linalool， AFB₁ solution （1 mg·kg^-1， dissolved in saline） was intraperitoneally injected for two consecutive days to induce acute liver injury in rats. Samples were collected and processed 14 days after model establishment. Pathological changes in liver tissue of rats were observed using Hematoxylin-eosin（HE） staining and Masson staining. Biochemical detection was performed to measure the levels of alanine transaminase（ALT）， aspartate transaminase（AST）， γ-glutamyl transferase（GGT）， lactate dehydrogenase（LDH）， alkaline phosphatase（ALP）， total bilirubin（TBil）， direct bilirubin（DBil）， indirect bilirubin（IBil）， malondialdehyde（MDA）， superoxidedismutase（SOD）， catalase（CAT） ， glutathione（GSH）， Fe³⁺， and Fe²⁺ in the liver tissue. Western blot was adopted to assess protein expression levels of nuclear factor-erythroid 2-related factor 2（Nrf2） and heme oxygenase-1（HO-1）. Molecular docking was performed to verify the binding between linalool and key proteins of the Nrf2/HO-1 signaling pathway. Molecular dynamics techniques were used to confirm the stability and affinity of linalool binding with key proteins of the Nrf2/HO-1 signaling pathway. ResultPathological results showed that compared to that in the AFB₁ group， the liver structure in the linalool group tended to be normal， with a significant decrease in blue collagen fibers. The linalool group exhibited significantly reduced levels of ALT， AST， GGT， LDH， ALP， TBil， DBil， and IBil （P<0.01）， Fe³⁺ and Fe²⁺ content， and oxidative stress marker MDA （P<0.01）. The levels of antioxidants SOD， CAT， and GSH significantly increased （P<0.01）. Molecular docking showed a molecular docking energy between linalool and Nrf2 and HO-1 targets of -5.495 6 and -5.199 4 kcal·mol^-1（1 cal≈4.186 J）， respectively. Molecular dynamics results indicated strong affinity in the binding of linalool with Nrf2 and HO-1. Western blot revealed a significant increase in Nrf2 protein expression （P<0.05） and a decrease in HO-1 protein expression （P<0.01） in the linalool group. ConclusionLinalool may protect against AFB₁-induced acute liver injury by modulating the Nrf2/HO-1 ferroptosis signaling pathway to inhibit liver cell ferroptosis and regulate hepatic oxidative stress levels.

ObjectiveMetabolomics was utilized to investigate the preventive effect of notoginseng total saponins（NTS） on aspirin（acetyl salicylic acid， ASA）-induced small bowel injury in rats. MethodFifty male SD rats were randomly divided into normal and model groups， NTS high-dose and low-dose groups（62.5， 31.25 mg·kg^-1）， and positive drug group（omeprazole 2.08 mg·kg^-1+rebamipide 31.25 mg·kg^-1）， with 10 rats in each group. Except for the normal group， rats in other groups were given ASA enteric-coated pellets 10.41 mg·kg^-1 daily to establish a small intestine injury model. On this basis， each medication group was gavaged daily with the corresponding dose of drug， and the normal group and the model group were gavaged with an equal amount of drinking water. Changes in body mass and fecal characteristics of rats were recorded and scored during the period. After 14 weeks of administration， small intestinal tissues of each group were taken for hematoxylin-eosin（HE） staining， scanning electron microscopy to observe the damage， and the apparent damage of small intestine was scored. Serum from rats in the normal group， the model group， and the NTS high-dose group was taken and analyzed for metabolomics by ultra-performance liquid chromatography-quadrupole-electrostatic field orbitrap high-resolution mass spectrometry（UPLC-Q-Exactive Orbitrap MS）， and the data were processed by multivariate statistical analysis， the potential biomarkers were screened by variable importance in the projection（VIP） value≥1.0， fold change（FC）≥1.5 or ≤0.6 and t-test P<0.05， and pathway enrichment analysis of differential metabolites was performed in conjunction with Human Metabolome Database（HMDB） and Kyoto Encyclopedia of Genes and Genomes（KEGG）. ResultAfter 14 weeks of administration， the average body mass gain of the model group was lower than that of the normal group， and the NTS high-dose group was close to that of the normal group. Compared with the normal group， the fecal character score of rats in the model group was significantly increased（P<0.05）， and compared with the model group， the scores of the positive drug group and the NTS high-dose group were reduced， but the difference was not statistically significant. HE staining and scanning electron microscopy results showed that NTS could significantly improve ASA-induced small intestinal injury， compared with the normal group， the small bowel injury score of the model group was significantly increased（P<0.01）， compared with the model group， the small bowel injury scores of the NTS low and high dose groups were significantly reduced（P<0.05， P<0.01）. Serum metabolomics screened a total of 75 differential metabolites between the normal group and the model group， of which 55 were up-regulated and 20 were down-regulated， 76 differential metabolites between the model group and the NTS groups， of which 14 were up-regulated and 62 were down-regulated. NTS could modulate three differential metabolites（salicylic acid， 3-hydroxybenzoic acid and 4-hydroxybenzoic acid）， which were involved in 3 metabolic pathways， namely， the bile secretion， the biosynthesis of folic acid， and the biosynthesis of phenylalanine， tyrosine and tryptophan. ConclusionNTS can prevent ASA-induced small bowel injury， and the underlying mechanism may be related to the regulation of bile secretion and amino acid metabolic pathways in rats.