Uncovering the crystallography and formation mechanism of nanoscale clusters in Sb-rich SPPs of a p-type (Bi, Sb)2Te3 alloy.

Considering that the crystallographic characteristics of the Sb-rich secondary phase particles (SPPs) greatly affect the thermoelectric properties of Bi2Te3 based materials, it is of great significance to explore the mechanism behind the Sb-rich SPPs in the p-type (Bi, Sb)2Te3 material. Here a conventional TEM technique was used to characterize the composition, size and distribution of Sb-rich SPPs in a spark plasma sintered p-type (Bi, Sb)2Te3 alloy. The results indicated that two different morphologies of Sb-rich SPPs including elongated and circular Sb-rich SPPs were frequently observed. Combined with high-resolution transmission electron microscopy, this work provides atomic-scale evidence for the formation mechanism behind the Sb-rich SPPs in the (Bi, Sb)2Te3 material.

The association between systemic inflammation markers and paroxysmal atrial fibrillation.

BACKGROUND: Systemic inflammation markers have recently been identified as being associated with cardiac disorders. However, limited research has been conducted to estimate the pre-diagnostic associations between these markers and paroxysmal atrial fibrillation (PAF). Our aim is to identify potential biomarkers for early detection of PAF. METHODS: 91 participants in the PAF group and 97 participants in the non-PAF group were included in this study. We investigated the correlations between three systemic inflammation markers, namely the systemic immune inflammation index (SII), system inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI), and PAF. RESULTS: The proportion of patients with PAF gradually increased with increasing logSII, logSIRI, and logAISI tertiles. Compared to those in the lowest tertiles, the PAF risks in the highest logSII and logSIRI tertiles were 3.2-fold and 2.9-fold, respectively. Conversely, there was no significant correlation observed between logAISI and PAF risk within the highest tertile of logAISI. The restricted cubic splines (RCS) analysis revealed a non-linear relationship between the elevation of systemic inflammation markers and PAF risk. Specifically, the incidence of PAF is respectively increased by 56%, 95%, and 150% for each standard deviation increase in these variables. The ROC curve analysis of logSII, logSIRI and logAISI showed that they had AUC of 0.6, 0.7 and 0.6, respectively. It also demonstrated favorable sensitivity and specificity of these systemic inflammation markers in detecting the presence of PAF. CONCLUSIONS: In conclusion, our study reveals significant positive correlations between SII, SIRI, and AISI with the incidence of PAF.

Transitional structure of {0001} twin in a deformed p-type (Bi,Sb)2Te3 alloy: a direct experimental basis for understanding the twinning mechanism.

Twin boundaries provide a strong phonon scattering center to hinder the lattice thermal conductivity in thermoelectric materials, but the underlying evolution process of deformation twinning remains to be figured out. By applying atomic resolution transmission electron microscope (TEM) observations, a novel type of transitional structure of {0001} twin was observed, for the first time, in the p-type (Bi,Sb)2Te3 alloy subjected to three-point bending deformation. The transformation from matrix to (0001) twin can be realized by the following path: matrix → transitional twin → (0001) twin, and this process was completed by the gliding of a total of four partial dislocations (b1 = 1/3[011̄0]) extended in the different (0001) planes. This new finding here will shed light on the nucleation and growth of deformation twins in the p-type (Bi, Sb)2Te3 alloy.

The association between systemic inflammation markers and the prevalence of hypertension.

BACKGROUND: We conducted a large-scale epidemiological analysis to investigate the associations between systemic inflammation markers and hypertension prevalence. Our aim is to identify potential biomarkers for early detection of hypertension. METHODS: A cross-sectional study with 119664 individuals from the National Health and Nutrition Examination Survey was performed. We investigated the associations between three systemic inflammation markers, namely the systemic immune inflammation index (SII), system inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI), and the prevalence of hypertension. RESULTS: The prevalence rates of hypertension gradually increased with increasing logSII, logSIRI, and logAISI quartiles. In continuous analyses, each unit increase in logSII, logSIRI, and logAISI was associated with a 20.3%, 20.1%, and 23.7% increased risk of hypertension. Compared to those in the lowest quartiles, the hypertension risks for subjects in the highest logSII, logSIRI, and logAISI quartiles were 1.114-fold,1.143-fold, and 1.186-fold. The restricted cubic splines (RCS) analysis revealed a non-linear relationship between the elevation of systemic inflammation markers and hypertension prevalence. Specifically, a per standard deviation increase in any of these variables is associated with a respective 9%, 16%, and 11% increase in hypertension prevalence. CONCLUSION: Our cross-sectional study reveals significant positive correlations between SII, SIRI, and AISI with the prevalence of hypertension.

5-Lipoxygenase Contributes to Benzo[a]pyrene-Induced Cytotoxicity and DNA Damage in Human Bronchial Epithelial Cells.

Metabolic activation of indirect-acting carcinogens in target organs is a recognized mechanism of carcinogenesis. This study aimed to determine the role of benzo[a]pyrene (BaP) metabolism enzymes lipoxygenase (LOX), cytochrome P4501A1 (CYP1A1), and prostaglandin synthetase (PGS) in the cytotoxicity and DNA damage induced by BaP in the human tracheobronchial epithelial cells (HBECs) using RNA interference strategy and metabolic enzyme inhibitors. Our results showed that in three epithelial cell lines (HBE, HTR-8/SVneo, and HaCat), BaP significantly upregulated 5-LOX protein expression. 15-LOX-2 expression also increased with increasing BaP concentration, but the change was less pronounced than that of 5-LOX. BaP caused significant cytotoxicity, DNA strand breaks, and 8-hydroxy-2'-deoxyguanosine formation in HBE, which was inhibited by 5-LOXshRNA, a specific inhibitor of 5-LOX (AA861), the CYP1A1 inhibitor α-naphthoflavone, and the PGS inhibitor naproxen. The protective effects of 5-LOXshRNA were stronger than AA861, naproxen and α-naphthoflavone. We conclude that BaP may be activated more by 5-LOX than by CYP1A1 and PGS to produce cytotoxicity and DNA damage in HBE.

Antiviral Bafilomycins from a Feces-Inhabiting Streptomyces sp.

A new bafilomycin derivative (1) and another seven known bafilomycins (2-8) were isolated from feces-derived Streptomyces sp. HTL16. The structure of 1 was elucidated by 1D and 2D NMR spectroscopic analysis. Biological testing demonstrated that these bafilomycins exhibited potent antiviral activities against the influenza A and SARS-CoV-2 viruses, with IC50 values in the nanomolar range, by inhibiting the activity of endosomal ATP-driven proton pumps.

Secondary Metabolites with Cytotoxic Activities from Streptomyces sp. BM-8 Isolated from the Feces of Equusquagga.

A new aliphatic acid, compound 1, together with six known metabolites, including nonactic acid (2), homononactic acid (3), ethyl homononactate (4), homononactylhomononactate (5), valinomycin (6), and cyclo-(Pro-Leu) (7), was isolated from the culture broth of Streptomyces sp. BM-8, an actinobacterial strain isolated from the feces of Equus quagga. The structures of these compounds were established by analyses of spectroscopic data, including 1D and 2D nuclear magnetic resonance spectra (NMR), as well as by HR-ESI-MS spectrometry and chemical derivative analyses. Additionally, a serial analogue of nonactic acid and homononacticacid (8-21) was synthesized. The cytotoxicity of 1-21 wastested against a panel of cancer cell lines, such as HT-29, MCF-7, A375 and K562, with MTT assay. In addition, the cytotoxicity tests revealed that 1 was less cytotoxic toward a panel of cancerous cells, as compared with valinomycin (6).

Elevated Homocysteine Levels Associated with Atrial Fibrillation and Recurrent Atrial Fibrillation.

There is increasing evidence linking plasma homocysteine levels and atrial fibrillation (AF). The association between an elevated level of plasma homocysteine and AF was examined by meta-analysis in this study.The PubMed and ScienceDirect databases until August 2019 were utilized to collect previous literature on homocysteine and the potential relation to AF. The pooled effects were evaluated depending on standardized mean differences (SMDs) or odds ratios (ORs) with 95% confidence intervals (CIs), and the calculation was performed using Stata 12 software.A total of 11 validated articles were included in the meta-analysis. For pooled effect, the results confirmed that AF patients had higher homocysteine levels than control subjects (SMD: 0.58, 95%CI: 0.09-1.06). Compared with control subjects, homocysteine levels were higher in paroxysmal AF (SMD: 0.45, 95%CI: 0.18-0.72) and persistent AF patients (SMD: 1.21, 95%CI: 0.50-1.92). The pooled analysis suggested that patients with elevated homocysteine levels had markedly higher risk of AF compared with lower homocysteine levels in the categorical variable (OR: 2.21, 95%CI: 1.16-4.21) and continuous variable analyses (OR: 1.13, 95%CI: 1.00-1.27), respectively. In addition, the pooled analysis indicated that recurrent AF patients had significantly higher homocysteine levels than those without recurrence (SMD: 0.65, 95%CI: 0.42-0.88). The pooled analysis of the categorical variables indicated that elevated homocysteine levels were associated with increased risk of AF recurrence (OR: 3.81, 95%CI: 3.11-4.68). However, the association was weak in the pooled analysis of continuous variables (OR: 1.88, 95%CI: 0.74-4.81).Our meta-analysis identified that plasma homocysteine levels were significantly elevated in AF and recurrent AF patients. Elevated homocysteine is associated with increased risk of AF and AF recurrence.

Lipoxygenase Protein Expression and Its Effect on Oxidative Stress Caused by Benzidine in Normal Human Urothelial Cell Lines.

Metabolic activation of indirect-acting carcinogens in the target organ is an effective mechanism of carcinogenesis. Lipoxygenase (LOX) can co-oxidize the bladder carcinogen benzidine (BZ). However, it is not entirely clear whether BZ is activated and which enzyme is involved in its activation in bladder epithelial cells. Our results showed that BZ induced 5-LOX protein expression but had no significant influence on the expression of 15-LOX-2, CYP1B1, and CYP2E1 in SV-40 immortalized human uroepithelial SV-HUC-1 cells. BZ induced oxidative stress in SV-HUC-1 cells by increasing reactive oxygen species (ROS) and malondialdehyde levels significantly in the 100 and 200 µmol/L-BZ-treated groups and decreased the level of the antioxidant reduced glutathione significantly at 200 µmol/L BZ. Concurrently, the activity of catalase was increased, while the activity of superoxide dismutase was increased at 50 µmol/L BZ but gradually decreased with increasing concentrations of BZ ( P < 0.05). However, the oxidative stress and damage in SV-HUC-1 cells caused by BZ were effectively inhibited by the 5-LOX-specific inhibitor AA861 at 10 µmol/L. Thus, 5-LOX is probably the major LOX isozyme to co-oxidize exogenous chemicals in SV-HUC-1 cells. AA861 has a protective effect on the oxidative stress and damage induced by BZ in SV-HUC-1 cells. We conclude that BZ can be activated by 5-LOX to produce ROS and oxidative stress, which may be associated with bladder cancer caused by BZ.

[Progress in study on the role of metabolomics in toxic effects of environmental pollutants and the underlying mechanism].

Metabolomics methods were applied in the study of the toxicity of environmental pollutants. It has been shown that exposure to heavy metals such as mercury, arsenic, cadmium, chromium and lead could cause significant changes in energy, lipids, nucleic acids and amino acids in mammalian cells. After exposure to benzo(a)pyrene [B(a)P], the glands of Pinctada pumila could produce various changes, such as energy metabolic disorder, cell damage, signal transduction disorder, oxidative stress and osmotic disorder. Persistent organic compounds polychlorinated biphenyls (PCBs) could exert toxic effects on Zebrafish embryos through affecting amino acid metabolism, DNA and protein methylation and biosynthesis. After exposure to endocrine disruptors, such as nonylphenol, octylenediester phthalate and bisphenol propane, goldfish showed energy, lipid and nucleic acid metabolic disorders.

[Relationship between the gene polymorphisms of oxidative metabolism enzyme of exogenous chemicals and the susceptibility to neoplasms].

The gene polymorphisms of human being will cause abnormality in the expression of corresponding gene, which is closely related to the physiological function and disease. Cytochrome P450, cyclooxygenase and lipoxygenase are vital enzymes that mediated the oxidative metabolism process for exogenous chemicals, and play important roles in activating the indirect carcinogens and metabolizing clinical drug; the gene polymorphisms of these enzymes can change the expression and activity of enzymes, affect the metabolic transformation of carcinogens, and then give rise to difference in the susceptibility to neoplasms. Studying the relationship between the gene polymorphisms of oxidative metabolism enzyme for endogenous and exogenous chemicals and the susceptibility to neoplasms can provide scientific basis for probing into the genetic markers and the pathogenesis of neoplasms.

Regioselective ortho-trifluoromethylthiolation of 2-arylbenzo[d]thiazole via tandem substrate-assisted C-H iodination and trifluoromethylthiolation.

A mild and efficient tandem benzo[d]thiazole directed C-H iodination and trifluoromethylthiolation for the synthesis of ortho-trifluoromethylthiolated 2-arylbenzo[d]thiazoles have been developed using AgSCF3 as a coupling partner. The reaction exhibits a diverse array of functional group tolerance giving the desired products in good to excellent yields. Regioselective trifluoromethylthiolation was observed at the less sterically hindered site when the phenyl ring of the substrate possesses a methyl group at its meta position.

[Expression of 5-lipoxygenase in human tissues and its association with disease].

5-Lipoxygenase, one of lipoxygenase isozymes, is a well-studied oxidative metabolism enzyme. It widely exists in various human tissues and cells, participates in the oxidative metabolism of endogenous and exogenous chemicals, and produces a variety of metabolites, all of which contribute to the occurrence of human diseases, such as inflammation, asthma, atherosclerosis, and tumor and so on. The expression of 5-lipoxygenase is at low level in normal human tissues while at high level in abnormal tissues. 5-Lipoxygenase is closely related to many kinds of diseases in human ovary, brain, cardiovascular system, lung, liver, pancreas and other tissues. The abnormal expression of 5-lipoxygenase tends to promote the development of the disease.

DNA-PKcs associates with PLK1 and is involved in proper chromosome segregation and cytokinesis.

Accurate mitotic regulation is as important as intrinsic DNA repair for maintaining genomic stability. It is believed that these two cellular mechanisms are interconnected with DNA damage. DNA-PKcs is a critical component of the non-homologous end-joining pathway of DNA double-stranded break repair, and it was recently discovered to be involved in mitotic processing. However, the underlying mechanism of DNA-PKcs action in mitotic control is unknown. Here, we demonstrated that depletion of DNA-PKcs led to the dysregulation of mitotic progression in response to DNA damage, which eventually resulted in multiple failures, including failure to segregate sister chromatids and failure to complete cytokinesis, with daughter cells becoming fused again. The depletion of DNA-PKcs resulted in a notable failure of cytokinesis, with a high incidence of multinucleated cells. There were also cytoplasmic bridges containing DNA that continuously connected the daughter cells after DNA damage was induced. Phosphorylated DNA-PKcs (T2609) colocalizes with PLK1 throughout mitosis, including at the centrosomes from prophase to anaphase and at the kinetochores from prometaphase to metaphase, with accumulation at the midbody during cytokinesis. Importantly, DNA-PKcs was found to associate with PLK1 in the mitotic phase, and the depletion of DNA-PKcs resulted in the overexpression of PLK1 due to increased protein stability. However, deficiency in DNA-PKcs attenuated the recruitment of phosphorylated PLK1 to the midbody but not to the kinetochores and centrosomes. Our results demonstrate the functional association of DNA-PKcs with PLK1, especially in chromosomal segregation and cytokinesis control.

RNA Interference Protects Against 5-Lipoxygenase-Induced Cocarcinogen, Benzidine, Oxidation and Cytotoxicity in Human Tracheobronchial Epithelial Cells.

Lipoxygenase (LOX)-catalyzed cooxidation of the human carcinogen benzidine (BZD) has been shown in in vitro enzyme systems. This study aimed to determine whether BZD could be activated by arachidonate 5-lipoxygenase (ALOX5) in the human tracheobronchial epithelial cells (HBECs) using RNA interference strategy and a 5-LOX-specific inhibitor, AA861. We show that the soybean LOX catalyzed the cooxidation of BZD, generating BZD diimine. Benzidine induced expression of ALOX5 messenger RNA and 5-LOX protein in HBECs, and significantly decreased cell proliferation, but enhanced DNA damage and apoptosis in HBECs which were significantly inhibited by lentiviral-mediated small hairpin RNA-knockdown of ALOX5 and by AA861. Thus, BZD could upregulate the expression of ALOX5 in HBECs, while inhibition of the protein or gene expression or enzyme activity could prevent BZD-induced cytotoxicity and DNA damage in HBECs, which might be caused by the 5-LOX-catalyzed oxidative activation of BZD.

Effect of dapagliflozin on left ventricular structure and function in patients with non-ischemic dilated cardiomyopathy: An observational study.

Non-ischemic dilated cardiomyopathy (NIDCM) is characterized by left ventricular dilatation and contractile dysfunction with severe morbidity and mortality. Sodium glucose cotransporter type 2 (SGLT2) inhibitors significantly reduce cardiovascular events for heart failure patients. We performed to investigate the impact of combined administration of SGLT2 inhibitors on cardiac structure and function in NIDCM patients undergoing conventional therapy. A total of 50 newly diagnosed NIDCM patients received conventional medical therapy, with 23 receiving dapagliflozin 10mg/day in addition (SGLT2i group) and the remaining 27 only receiving conventional therapy (non-SGLT2i group). After 12 months outpatient follow-up, NIDCM patients treated with conventional therapy alone showed a significant reduction of left ventricular end-diastolic dimensions (LVEDd), left ventricular end-systolic dimensions (LVESd), left ventricular end-diastolic volumes (LVEDV), left ventricular end-systolic volumes (LVESV), left ventricular end-diastolic volume index (LVEDVi) and left ventricular end-systolic volume index (LVESVi), while an increase in fractional shortening (FS) and left ventricular ejection fraction (LVEF). Patients receiving dapagliflozin combined with conventional treatment also demonstrated a significant reduction in left ventricular dimensions and volumes, and a marked increase in cardiac function. In non-SGLT2i groups, the % change in LVEDd, LVESd, LVEDV, LVESV, LVEDVi, LVESVi, FS and LVEF was -2.8%, -4.6%, -6.2%, -10.1%, -6.1%, -10.1%, +9.7%, +11%. A greater absolute % fall in left ventricular volume in SGLT2i groups compared to non-SGLT2i groups resulted in a significant improvement in cardiac function. The results showed that SGLT2i combined with conventional therapy has a better beneficial effect on left ventricular volumes and cardiac function in NIDCM patients.

Micromechanical modelling for bending behaviour of novel bioinspired alumina-based dental composites.

The clinical failure mode of dental crown ceramics involves radial cracking at the interface, driven by the surface tension generated from the flexure of the ceramic layer on the subsurface. This results in a reduced lifespan for most all-ceramic dental crowns. Therefore, investigating optimal material combinations to reduce stress concentration in dental crown materials has become crucial for future successful clinical applications. The anisotropic complex structures of natural materials, such as nacre, could potentially create suitable strong and damage-resistant materials. Their imitation of natural structural optimisation and mechanical functionality at both the macro- and micro-levels minimises weaknesses in dental crowns. This research aims to optimise cost-effective, freeze-casted bioinspired composites for the manufacture of novel, strong, and tough ceramic-based dental crowns. To this end, multilayer alumina (Al2O3) composites with four different polymer phases were tested to evaluate their bending behaviour and determine their flexural strength. A computational model was developed and validated against the experimental results. This model includes Al2O3 layers that undergo gentle compression and distribute stress, while the polymer layers act as stress relievers, undergoing plastic deformation to reduce stress concentration. Based on the experimental data and numerical modelling, it was concluded that these composites exhibit variability in mechanical properties, primarily due to differences in microstructures and their flexural strength. Furthermore, the findings suggest that bioinspired Al2O3-based composites demonstrate promising deformation and strengthening behaviour, indicating potential for application in the dental field.

[Study on activation of benzo(a)pyrene and DNA damage mediated by lipoxygenase in human bronchial epithelial cells].

OBJECTIVE: The oxidation of benzo (a) pyrene mediated by 5-lipoxygenase (5-LOX) were investigated in HBE cells in order to provide further proof that lipoxygenase is the alternative pathway for the oxidation of xenobiotics. METHODS: Enzymic experiment: Soybean lipoxygenase (SLO), substrate (benzo[a] pyrene) and other component react in the enzymic system and the reaction product are detected by spectrophotometry. At the same time, in vitro detect of benzo (a) pyrene-DNA adducts with a UV spectrophotometer and HPLC. Cellular experiment: After HBE cells exposure to different poison (B[a]P 4, 8, 16, 32, 64, 128µmol/L, AA-861, naproxen or α- naphthoflavone 0.1, 1, 10 µmol/L) for 24 hours, the effect of benzo (a) -pyrene on cell survival rate were assessed by reductions of tetrazolium dye (MTT) and flow cytometry in cultured HBE cells, and the protein expressions of 5-lipoxygenase in the cells are tested by western-blot, and the DNA damages by the single cell gel electrophoresis. And then, the effect of the specific inhibitor of 5-lipoxygenase (AA-861) on 5-lipoxygenase protein expression and DNA damage in the cells are detected. RESULTS: SLO can catalyze the co-oxidation of benzo (a) pyrene to generate benzo (a) pyrene-7,8-epoxide in the presence of hydrogen peroxide. GTP can inhibit the reaction , the IC50 value is 0.46 mg/L, the model equation is Probit (P) = 0.8985+2.6824 Log (dose). SLO can catalyze the co-oxidation of benzo (a) pyrene to generate a new product, but fail to form DNA adducts in vitro. HBE cell viability decreased with the benzo (a) pyrene concentration increased , but AA-861 and naproxen can inhibit it. Flow cytometry and single cell gel electrophoresis experiments show, Benzo (a) pyrene can induce 5-lipoxygenase protein expression, but AA-861 cannot in HBE. Benzo (a) pyrene causes toxic action and DNA damage in HBE, which can significantly inhibit by AA-861, the difference is statistically significant (P < 0.05). CONCLUSIONS: The co-oxidate of benzo (a) pyrene by 5-LOX turns into electrophiles that covalently bind to DNA and induce DNA damage, which can be significantly inhibited by AA-861.

Hypobaric hypoxia induces iron mobilization from liver and spleen and increases serum iron via activation of ghrelin/GHSR1a/MAPK signalling pathway in mice.

Hypobaric hypoxia (HH) exposure affects appetite and serum iron levels in both humans and animals. Thus, whether appetite-regulating ghrelin is involved in iron regulation under HH needs to be elucidated. In vivo, C57BL/6J mice were placed in a hypobaric chamber to establish a 6000-m-high altitude exposure animal model. In vitro, mouse primary hepatocytes and peritoneal macrophages were exposed to hypoxia (1% O2) to examine the effects of ghrelin on iron-regulating proteins. HH obviously reduced the body weight of mice and significantly increased the levels of erythrocytes, and also significantly enhanced the levels of serum iron and plasma ghrelin. However, iron content in the liver and spleen was decreased, while ferroportin (Fpn) expression was increased. Moreover, ghrelin significantly induced Fpn and pERK expression in both hepatocytes and macrophages under hypoxia, which were reversed by pretreatment with growth hormone secretagogue receptor 1a (GHSR1a) antagonist or pERK inhibitor. Our findings indicated that HH leads to decreased appetite and insufficient dietary intake, which may negatively regulate the levels of ghrelin. Furthermore, GHSR1a/ERK signalling pathway is further activated to upregulate the expression of Fpn, and then promoting iron mobilization both in the liver/hepatocytes and spleen/macrophages in mice. Thus, these results revealed that ghrelin may be a potential iron regulatory hormone, and raised the possibility of ghrelin as a promising therapeutic target against iron disorders under HH.

Phenolic compound SG-1 from Balanophora harlandii and its derivatives exert anti-influenza A virus activity via activation of the Nrf2/HO-1 pathway.

Influenza A virus (IAV) is one of the leading causes of respiratory illness and continues to cause pandemics around the world. Against this backdrop, drug resistance poses a challenge to existing antiviral drugs, and hence, there is an urgent need for developing new antiviral drugs. In this study, we obtained a phenolic compound SG-7, a derivative of natural compound 2-hydroxymethyl-1,4-hydroquinone, which exhibits inhibitory activity toward a panel of influenza viruses and has low cellular toxicity. Mechanistic studies have shown that SG-7 exerts its anti-IAV properties by acting on the virus itself and modulating host signaling pathways. Namely, SG-7 targets the HA2 subunit of hemagglutinin (HA) to block the fusion of viral-cellular membranes and inhibits IAV-induced oxidative stress and overexpression of pro-inflammatory factors by activating the Nrf2/HO-1 pathway and reducing NF-κB activation. In addition, SG-7 can enhance type I IFN antiviral response by inducing Nrf2 expression. Importantly, SG-7 showed the ability to inhibit viral replication in the lungs of IAV-infected mice and reduce their mortality. Therefore, SG-7 may be a promising lead compound for anti-influenza drug development.