Grassland degradation amplifies the negative effect of nitrogen enrichment on soil microbial community stability.

Although nitrogen (N) enrichment is known to threaten the temporal stability of aboveground net primary productivity, it remains unclear how it alters that of belowground microbial abundance and whether its impact can be regulated by grassland degradation. Using data from N enrichment experiments at temperate grasslands with no, moderate, severe, and extreme degradation degrees, we quantified the temporal stability of soil microbial abundance (hereafter 'microbial community stability') using the ratio of the mean quantitative PCR to its standard deviation over 4 years. Both bacterial and fungal community stability sharply decreased when N input exceeded 30 g N m-2 year-1 in non-degraded grasslands, whereas a reduction in this threshold occurred in degraded grasslands. Microbial species diversity, species asynchrony, and species associations jointly altered microbial community stability. Interestingly, the linkages between plant and microbial community stability were strengthened in degraded grasslands, suggesting that plants and soil microbes might depend on each other to keep stable communities in harsh environments. Our findings highlighted the importance of grassland degradation in regulating the responses of microbial community stability to N enrichment and provided experimental evidence for understanding the relationships between plant and microbial community stability.

Design, synthesis and evaluation of thieno[3,2-d]pyrimidine derivatives as novel potent CDK7 inhibitors.

The targeting of cyclin-dependent kinase 7 (CDK7) has become a highly desirable therapeutic approach in the field of oncology due to its dual role in regulating essential biological processes, encompassing cell cycle progression and transcriptional control. We have previously identified a highly selective thieno[3,2-d]pyrimidine-based CDK7 inhibitor with demonstrated efficacy and safety in animal model. In this study, we sought to optimize the thieno[3,2-d]pyrimidine core to discover a novel series of CDK7 inhibitors with improved potency and pharmacokinetic (PK) properties. Through extensive structure-activity relationship (SAR) studies, compound 20 has emerged as the lead candidate due to its potent inhibitory activity against CDK7 and remarkable efficacy on MDA-MB-453 cells, a representative triple negative breast cancer (TNBC) cell line. Furthermore, 20 has demonstrated favorable oral bioavailability and exhibited highly desirable pharmacokinetic (PK) properties, making it a promising lead candidate for further structural optimization.

Risk of heavy metal(loid) compositions in fine particulate matter on acute cardiovascular mortality: a poisson analysis in Anyang, China.

Fine particulate matter (PM2.5) is a risk factor of cardiovascular disease. Associations between PM2.5 compositions and cardiovascular disease are a point of special interest but inconsistent. This study aimed to explore the cardiovascular effects of heavy metal(loid) compositions in PM2.5. Data for mortality, air pollutants and meteorological factors in Anyang, China from 2017 to 2021 were collected. Heavy metal(loid) in PM2.5 were monitored and examined monthly. A Case-crossover design was applied to the estimated data set. The interquartile range increase in cadmium (Cd), antimony (Sb) and arsenic (As) at lag 1 was associated with increment of 8.1% (95% CI: 3.3, 13.2), 4.8% (95% CI: 0.2, 9.5) and 3.5% (95% CI: 1.1, 6.0) cardiovascular mortality. Selenium in lag 2 was inversely associated with cerebrovascular mortality (RR = 0.920 95% CI: 0.862, 0.983). Current-day exposure of aluminum was positively associated with mortality from ischemic heart disease (RR = 1.083 95% CI: 1.001, 1.172). Stratified analysis indicated sex, age and season modified the cardiovascular effects of As (P < 0.05). Our study reveals that heavy metal(loid) play key roles in adverse effects of PM2.5. Cd, Sb and As were significant risk factors of cardiovascular mortality. These findings have potential implications for accurate air pollutants control and management to improve public health benefits.

Soil fertility shifts the relative importance of saprotrophic and mycorrhizal fungi for maintaining ecosystem stability.

Soil microbial communities are essential for regulating the dynamics of plant productivity. However, how soil microbes mediate temporal stability of plant productivity at large scales across various soil fertility conditions remains unclear. Here, we combined a regional survey of 51 sites in the temperate grasslands of northern China with a global grassland survey of 120 sites to assess the potential roles of soil microbial diversity in regulating ecosystem stability. The temporal stability of plant productivity was quantified as the ratio of the mean normalized difference vegetation index to its standard deviation. Soil fungal diversity, but not bacterial diversity, was positively associated with ecosystem stability, and particular fungal functional groups determined ecosystem stability under contrasting conditions of soil fertility. The richness of soil fungal saprobes was positively correlated with ecosystem stability under high-fertility conditions, while a positive relationship was observed with the richness of mycorrhizal fungi under low-fertility conditions. These relationships were maintained after accounting for plant diversity and environmental factors. Our findings highlight the essential role of fungal diversity in maintaining stable grassland productivity, and suggest that future studies incorporating fungal functional groups into biodiversity-stability relationships will advance our understanding of their linkages under different fertility conditions.

LiBF4-Promoted Aromatic Fluorodetriazenation under Mild Conditions.

An efficient and mild fluorination method through LiBF4-promoted aromatic fluorodetriazenation of 3,3-dimethyl-1-aryltriazenes is developed. The reaction proceeds smoothly and tends to complete within 2 h in the absence of a protic acid or strong Lewis acid. This method tolerates a wide range of functional groups and affords the aryl fluoride products in moderate to excellent yields.

Amelioration of metabolic disorders in H9C2 cardiomyocytes induced by PM2.5 treated with vitamin C.

OBJECTIVE: Particulate matter with an aerodynamic diameter ≤2.5 µm (PM2.5) is a public health risk. We investigate PM2.5 on metabolites in cardiomyocytes and the influence of vitamin C on PM2.5 toxicity. MATERIALS AND METHODS: For 24 hours, H9C2 were exposed to various concentrations of PM2.5 (0, 100, 200, 400, 800 µg/ml), after which the levels of reactive oxygen species (ROS) and cell viability were measured using the cell counting kit-8 (CCK-8) and 2',7'-dichlorofluoresceindiacetate (DCFH2-DA), respectively. H9C2 were treated with PM2.5 (200 µg/ml) in the presence or absence of vitamin C (40 µmol/L). mRNA levels of interleukin 6(IL-6), caspase-3, fatty acid-binding protein 3 (FABP3), and hemeoxygenase-1 (HO-1) were investigated by quantitative reverse-transcription polymerase chain reaction. Non-targeted metabolomics by LC-MS/MS was applied to evaluate the metabolic profile in the cell. RESULTS: Results revealed a concentration-dependent reduction in cell viability, death, ROS, and increased expression of caspase-3, FABP3, and IL-6. In total, 15 metabolites exhibited significant differential expression (FC > 2, p < 0.05) between the control and PM2.5 group. In the PM2.5 group, lysophosphatidylcholines (LysoPC,3/3) were upregulated, whereas amino acids (5/5), amino acid analogues (3/3), and other acids and derivatives (4/4) were downregulated. PM2.5 toxicity was lessened by vitamin C. It reduced PM2.5-induced elevation of LysoPC (16:0), LysoPC (16:1), and LysoPC (18:1). DISCUSSION AND CONCLUSIONS: PM2.5 induces metabolic disorders in H9C2 cardiomyocytes that can be ameliorated by treatment with vitamin C.

Inhibition of semaphorin-3a alleviates lipopolysaccharide-induced vascular injury.

Alleviating vascular injury improves the prognosis of atherosclerosis. Semaphorin-3a (Sema3A) is a special membrane-associated secreted protein with various biological properties, like pro-inflammation, anti-tumor and et al. This study aims to investigate the effects of inhibition of Sema3A on lipopolysaccharide (LPS)-induced vascular injury in mice. The mice were randomized into three groups: control, LPS, and LPS + siRNA. Mice in the combined group were given siRNA through fast tail vein injection, then LPS was injected intraperitoneally 7 days later, finally the mice were euthanized 24 h later. Vascular function and structure were assessed by vascular injury biomarkers and relevant stainings. LPS-induced vascular dysfunction and pathological injury were substantially improved by inhibition of Sema3A. Western blot and quantitative real-time polymerase chain reaction assays were used for investigating molecular pathways. The relevant proteins of vascular endothelial cells activation, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), increased after LPS stimulation, while these effects were reversed by inhibition of Sema3A. The levels of inflammatory cytokines (IL-1ß, IL-6 and NLRP3) were upregulated after LPS stimulation, however, inhibition of Sema3A reversed it through NF-κB and MAPKs signaling pathways involvement. Moreover, inhibition of Sema3A alleviated LPS-induced oxidative stress, evidenced by a decrease in total reactive oxygen species and an increase in antioxidant protein of SOD-1. The results showed that inhibition of Sema3A protects against LPS-induced vascular injury by suppressing vascular endothelial cells activation, vascular inflammation, and vascular oxidative stress, implying that inhibition of Sema3A might be used as a therapeutic strategy for septic vascular injury or atherosclerosis.

Identification of potential pathways associated with indole-3-butyric acid in citrus bud germination via transcriptomic analysis.

Indole-3-butyric acid (IBA) is widely used to encourage root development in cuttings of general field crops, vegetables, forest trees, fruit trees, and flowers. However, previous studies reported that IBA inhibited the germination of citrus buds via an unknown molecular mechanism. This study aimed to unravel the regulatory mechanisms underlying this inhibition. Citrus apical buds were sprayed with 100 mg ⋅ L-1 IBA. Subsequently, the plant hormone levels were analyzed, and transcriptomic analysis was performed. The results identified 3325 upregulated genes and 2926 downregulated genes in the citrus apical buds. The gene set enrichment analysis method was used to determine the Gene Ontology related to the treatment. Genes were enriched into 157 sets, including 17 upregulated sets and 140 downregulated sets, after indole butyric acid treatment. The upregulated gene sets were related to glucose import, sugar transmembrane transporter activity, and photosynthesis. The downregulated genes were mainly related to the ribosomal subunit and cell cycle process under butyric acid treatment. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed the enrichment of 11 pathways. Of note, genes related to the ribosome and proteasome pathways were significantly downregulated. Only one pathway was significantly upregulated: the autophagy pathway. Overall, these results provided insights into the molecular mechanisms underpinning the IBA-mediated inhibition of citrus bud germination inhibition. Also, the study provided a large transcriptomics dataset that could be used for further research.

Risk Factors and Molecular Epidemiology of Complicated Intra-Abdominal Infections With Carbapenem-Resistant Enterobacteriaceae: A Multicenter Study in China.

BACKGROUND: Carbapenem-resistant Enterobacteriaceae (CRE) infections are associated with poor patient outcomes. Data on risk factors and molecular epidemiology of CRE in complicated intra-abdominal infections (cIAI) in China are limited. This study examined the risk factors of cIAI with CRE and the associated mortality based on carbapenem resistance mechanisms. METHODS: In this retrospective analysis, we identified 1024 cIAI patients hospitalized from January 1, 2013 to October 31, 2018 in 14 intensive care units in China. Thirty CRE isolates were genotyped to identify ß-lactamase-encoding genes. RESULTS: Escherichia coli (34.5%) and Klebsiella pneumoniae (21.2%) were the leading pathogens. Patients with hospital-acquired cIAI had a lower rate of E coli (26.0% vs 49.1%; P < .001) and higher rate of carbapenem-resistant Gram-negative bacteria (31.7% vs 18.8%; P = .002) than those with community-acquired cIAI. Of the isolates, 16.0% and 23.4% of Enterobacteriaceae and K pneumoniae, respectively, were resistant to carbapenem. Most carbapenemase-producing (CP)-CRE isolates carried blaKPC (80.9%), followed by blaNMD (19.1%). The 28-day mortality was 31.1% and 9.0% in patients with CRE vs non-CRE (P < .001). In-hospital mortality was 4.7-fold higher for CP-CRE vs non-CP-CRE infection (P = .049). Carbapenem-containing combinations did not significantly influence in-hospital mortality of CP and non-CP-CRE. The risk factors for 28-day mortality in CRE-cIAI included septic shock, antibiotic exposure during the preceding 30 days, and comorbidities. CONCLUSIONS: Klebsiella pneumoniae had the highest prevalence in CRE. Infection with CRE, especially CP-CRE, was associated with increased mortality in cIAI.

BST2 Promotes Tumor Growth via Multiple Pathways in Hepatocellular Carcinoma.

Bone marrow stromal antigen 2 (BST2) is a transmembrane glycoprotein and plays an essential role in innate immunity. Here we firstly found that BST2 expression was significantly elevated in hepatocellular carcinoma (HCC) tissues. High BST2 was closely related to the larger tumor size and more tumor number. Moreover, HCC patients with higher expression of BST2 had poorer overall survival and BST2 was identified as an independent unfavorable prognosis factor. Finally, we demonstrated that BST2 can promote proliferation capacity of tumor cells. In conclusion, HCC patients with higher BST2 expression were more predisposed to poorer clinical symptoms and unfavorable prognosis.

A novel mimovirus encoding ChgA10-19 peptide with PD-L1 induces T cell tolerance and ameliorates the severity of diabetes.

Related studies demonstrate that type 1 diabetes (T1D) is caused by ß-cell antigen specific autoreactive CD8+ T cells. ChgA has recently been identified as the autoantigen in NOD mice and T1D patients. Therefore, attenuating the activation of ChgA specific CD8+ T cells might be a promising target for T1D therapy. The negative co-stimulatory PD-L1 inhibits T cell mediated alloimmunity and induces tolerance. In this experiment, a novel mimovirus encoding ChgA10-19 peptide with PD-L1 was constructed. The NOD.ß2m null HHD mice were administrated with mimovirus transduced DCs. After immunization, the activation and proliferation of CD8+ T cells were detected, diabetes incidence and pancreatic tissue destruction were also analyzed. The results demonstrated that transduced DCs attenuated CD8+ T cell activation and proliferation. In addition, transduced DCs inhibited CD8+ T response to ChgA stimulation, and ameliorated the severity of diabetes. These data suggested that mimovirus transduced DCs might provide novel clues for T1D therapy.

[Analysis of association of genetic polymorphisms of microRNAs with ischemic stroke].

OBJECTIVE: To assess the association of single nucleotide polymorphisms of hsa-miR-196a2, hsa-miR-149, hsa-miR-146a, hsa-miR-499 with susceptibility to ischemic stroke. METHODS: Taqman-PCR and DNA sequencing assays were employed to determine the genotypes of the 4 loci among 510 patients and 523 controls. And their association with the disease was assessed. RESULTS: Analysis showed that smoking, diabetes, hypertension, BMI index and abnormal serum lipid metabolism were significantly associated with ischemic stroke, and that rs2910164 was significantly associated with the disease in codominant (CG vs. CC: P=0.002, OR=1.878, 95%CI=1.269-2.789), dominant (P=0.012, OR=1.325, 95%CI=1.110-1.580), recessive (P=0.008, OR=1.630, 95%CI=1.130-2.342) and allele (P=0.002, OR=1.449, 95%CI=1.210-1.731) genetic models. Stratified analysis further showed that the significant association only existed in population with smoking and hypertension. By contrast, no association was found between hsa-miR-196a2 rs11614913, hsa-miR-149 rs2292832 and hsa-miR-499 rs3746444 with the disease. CONCLUSION: Our study indicated that smoking, diabetes, hypertension, fat and hyperlipidemia are risk factors for ischemic stroke. Hsa-miR-146a rs2910164 is significantly associated with the disease in those with smoking and hypertension in Dongyang region and may be involved in the process of the disease. The G allele G, GG and CG+GG genotypes of the locus may underlie the susceptibility to the disease in Dongyang region.

Size-fitting effect for hybridization of DNA/mercaptohexanol mixed monolayers on gold.

In this article we proposed a simple hexagonal model for exploring the hybridization of thiol-modified probe DNA self-assembled monolayers (SAMs) on gold with target DNA molecules in solution. The size-fitting coefficient d(c)/d(t) from the model was used to discuss the principle for DNA optimal hybridization, where d(c) was the channel diameter among three adjacent probe DNA molecules on gold and dt was the gyration diameter of the target DNA molecules in solution. Experimentally we investigated the hybridization effect (hybridization efficiency H(E) and hybridization density H(D)) of thiol-modified probe DNA (DNA base amount m = 15, 25 or 35)/mercaptohexanol (MCH) mixed SAMs on gold in 1 M electrolyte solution by chronocoulometry (CC) and electrochemical impedance spectroscopy (EIS). The surface coverage Γ(m) of the probe DNA on gold was adjusted by changing the mixed concentration ratio of probe DNA with MCH (C(DNA)/C(MCH)) in the assembly solution. Results indicated that with the increase of C(DNA)/C(MCH), H(E) decreased gradually; H(D) first increased and then decreased, which arrived at the biggest at C(DNA)/C(MCH) = 1 for all the probe DNA/MCH mixed SAMs (m = 15, 25, 35). The optimal Γ(m) for achieving the biggest H(D) in DNA hybridization decreased with the increase of m from 15 to 35. The experimental conclusions obtained by CC and EIS measurements verified each other. Combining the simple model with our experimental results, we ascertained that d(c)/d(t) decreased with the increase of m, which showed a good linear relationship. These conclusions provided an important reference and guidance for controllably constructing DNA sensors with optimal performance.

Sophocarpine alleviates doxorubicin-induced heart injury by suppressing oxidative stress and apoptosis.

Doxorubicin (DOX) is an effective anti-tumor drug accompanied with many side effects, especially heart injury. To explore what effects of sophocarpine (SOP) on DOX-induced heart injury, this study conducted in vivo experiment and in vitro experiment, and the C57BL/6J mice and the H9C2 cells were used. The experimental methods used included echocardiography, enzyme-linked immunosorbent assay (ELISA), dihydroethidium (DHE) staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, western blotting and so on. Echocardiography showed that SOP alleviated DOX-induced cardiac dysfunction, as evidenced by the improvements of left ventricle ejection fraction and left ventricle fractional shortening. DOX caused upregulations of creatine kinase (CK), creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), while SOP reduced these indices. The relevant stainings showed that SOP reversed the increases of total superoxide level induced by DOX. DOX also contribute to a higher level of MDA and lower levels of SOD and GSH, but these changes were suppressed by SOP. DOX increased the pro-oxidative protein level of NOX-4 while decreased the anti-oxidative protein level of SOD-2, but SOP reversed these effects. In addition, this study further discovered that SOP inhibited the decreases of Nrf2 and HO-1 levels induced by DOX. The TUNEL staining revealed that SOP reduced the high degree of apoptosis induced by DOX. Besides, pro-apoptosis proteins like Bax, cleaved-caspase-3 and cytochrome-c upregulated while anti-apoptosis protein like Bcl-2 downregulated when challenged by DOX, but them were suppressed by SOP. These findings suggested that SOP could alleviate DOX-induced heart injury by suppressing oxidative stress and apoptosis, with molecular mechanism activating of the Nrf2/HO-1 signaling pathway.

The impact of superselective adrenal artery embolization on renal function in patients with primary aldosteronism: a prospective cohort study.

Superselective adrenal artery embolization (SAAE) is an effective treatment for patients with primary aldosteronism (PA). However, the impact of SAAE on renal function in the PA population remains uncertain. We investigated the estimated glomerular filtration rate (eGFR) and age, sex, body mass index, and diabetes-specific percentiles of eGFR residuals in 182 PA patients treated with SAAE in a prospective cohort from Nanchang SAAE in treating PA registry study. Data suggest that SAAE caused a significant decrease in eGFR from 91.9 ± 26.1 to 88.7 ± 24.1 ml/min/1.73 m2 (p < 0.05) after a median follow-up of 8 months in PA patients. Patients experienced a significant decrease in eGFR from 110.6 ± 18.9 to 103.8 ± 18.2 ml/min/1.73 m2 (p < 0.001) and a very slight increase from 71.1 ± 14.8 to 71.8 ± 17.8 ml/min/1.73 m2 (p = 0.770) with baseline eGFR ≥90 and <90 ml/min/1.73 m2, respectively. Patients with high eGFR residuals (glomerular hyperfiltration) experienced a significant decrease in their eGFR levels from 123.1 ± 22.6 to 105.0 ± 18.6 ml/min/1.73 m2 (p < 0.001). In contrast, there was no significant impact of SAAE on the eGFR of patients with normal or low eGFR residuals. The very early eGFR changes (24 h after SAAE) best predicted the effect of SAAE on eGFR changes after median of eight months in PA patients. On the whole, SAAE seems to have a beneficial impact on renal function in patients with PA, the results of which vary depending on the patient's baseline eGFR and glomerular hyperfiltration status.

Sensitive dual-signal detection and effective removal of tetracycline antibiotics in honey based on a hollow triple-metal organic framework nanozymes.

In this work, a colorimetric/fluorescent dual-signal mode sensor is proposed for the sensitive, selective and accurate detection and removal of tetracycline antibiotics (TCs). A triple-metal MOF of NiCoFe is successfully synthesized and controllable adjusted the shape of the hollow structure for the first time, and then modified with TCs aptamer. The as-prepared triple-atom MOF (apt-NiCoFe-MOF-74) exhibits well-defined hollow morphology, high crystallinity, and high surface areas endow their alluring adsorption and removal performances for TCs. More attractively, this triple-metal MOF show a good peroxidase-like activity and strong fluorescence property at 540 nm of apt-NiCoFe-MOF-74 when excitation wavelength was 370 nm. Inspire by this, a dual-signal output biosensor is constructed and the linear absorbance response is well correlated with wide range and low LOD for TCs. The biosensor provided an universal method with satisfactory sensitivity and accuracy for TCs analysis in real food samples.

A Novel PiGF@Diamond Color Converter with a Record Thermal Conductivity for Laser-Driven Projection Display.

High-brightness laser lighting is confronted with crucial challenges in developing laser-excitable color converting materials with effective heat dissipation and super optical performance. Herein, a novel composite of phosphor-in-glass film on transparent diamond (PiGF@diamond) is designed and fabricated via a facile low-temperature co-sintering strategy. The as-prepared La3Si6N11:Ce3+ (LSN:Ce) PiGF@diamond with well-retained optical properties of raw phosphor shows a record thermal conductivity of ≈599 W m-1 K-1, which is about 60 times higher than that of currently well-used PiGF@sapphire (≈10 W m-1 K-1). As a consequence, this color converter can bear laser power density up to 40.24 W mm-2 and a maximum luminance flux of 5602 lm without luminescence saturation due to efficient inhibition of laser-induced heat accumulation. By further supplementing red spectral component of CaAlSiN3:Eu2+ (CASN:Eu), the PiGF@diamond based white laser diode is successfully constructed, which can yield warm white light with a high color rendering index of 89.3 and find practical LD-driven applications. The findings will pave the way for realizing the commercial application of PiGF composite in laser lighting and display.

Dispel the Clouds and See the Sun: Influencing Factors and Multiple Paths of User Retention Intention Formation.

To achieve user retention through multifactor synergy, Internet enterprises must reduce costs and increase efficiency and sustainable development. In response to the dilemma that Internet companies are experiencing increasingly high user acquisition costs and serious user churn, this paper investigates a sample of 46,695 user reviews of nine product series from Xiaomi Ecological Chain. Case studies and qualitative comparative analysis are used to explore the influence mechanisms of quality of experience, brand trust, and brand attachment on users' retention intentions. Our findings are as follows. (1) Brand attachment alone is not necessary for high user retention intention, but user perception, cognition, and brand trust are necessary. (2) Quality of experience positively impacts brand trust, attachment, and user retention intention. Therefore, improving user perception and cognition is critical in generating high user retention intention. (3) Five configuration paths can achieve high user retention intention, while three configuration paths lead to low user retention intention, and there is an asymmetric relationship between these paths. Among them, the role of quality of experience-driven configuration paths in generating user retention intention is the most prominent. (4) User perception and cognition can substitute with brand trust and attachment in the substitution relationship between configuration paths. Our findings have important theoretical and practical implications for revealing the realization paths of high user retention intention in Internet companies and provide a new perspective for future research.

The protective effects of sophocarpine on sepsis-induced cardiomyopathy.

This investigation elucidates the impact of sophocarpine treatment on lipopolysaccharide (LPS) stimulated sepsis-induced cardiomyopathy (SIC) via in vivo and in vitro experiments. Echocardiography, ELISA, TUNEL, Western blotting experiments, and Hematoxylin/Eosin, Dihydroethidium, and Immunohistochemistry staining assays, were carried out to identify associated indicators. The echocardiography revealed that sophocarpine treatment alleviated LPS-induced cardiac dysfunction as indicated by fractional shortening shortened and improved ejection fraction. Heart injury biomarkers, such as creatine kinase, lactate dehydrogenase, and creatine kinase-MB, were assessed, and indicated that sophocarpine treatment could alleviate LPS-induced upregulation of these indices. Furthermore, different experimental protocols revealed that sophocarpine treatment inhibits LPS-induced pathological alterations and decreases LPS-stimulated inflammatory cytokines, IL-1ß, monocyte chemoattractant protein-1, IL-6, NOD-like receptor protein-3, and TNF-α, increase. Apoptotic proteins such as cytochrome-c, Bax, and cleaved-caspase-3 were increased, and Bcl-2 was alleviated after LPS stimulation; however, these effects were inhibited by sophocarpine treatment. Decreased antioxidant proteins [superoxide dismutase-1 (SOD-1) and SOD-2] induced by LPS stimulation were upregulated by sophocarpine treatment. LPS upregulated autophagic proteins such as Beclin-1 and the ratio of microtubule-associated protein 1A/1B-light chain 3 (LC3)-II/LC3-I and downregulated sequestosome 1 (SQSTM1, or P62), sophocarpine therapy reversed these effects. Moreover, it was indicated that sophocarpine treatment inhibited the Toll-like receptor-4 (TLR-4)/nuclear transcription factor-kappa B (NF-κB) signaling pathway and activated nuclear factor erythroid 2-related factor-2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In conclusion, sophocarpine treatment could alleviate LPS-trigger SIC by repressing oxidative stress, autophagy, inflammation, and apoptosis via TLR-4/NF-κB inhibition and Nrf2/HO-1 signaling pathway activation, implicating the potential of sophocarpine as a new therapeutic approach against SIC.