ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2022
·
IF 7.129
Tianmeng Zhang,Zhuhua Dong,Feixue Liu,Enzhuang Pan,Nana He,Fenfen Ma,Guanglu Wang,Yan Wang,Jingquan Dong
Avermectin, a "low toxicity insecticide", has been widely used in recent years, but its non-target toxicity, especially to aquatic organisms, has been neglected. In this study, we evaluated the neurotoxic effects of avermectin on carp by establishing a 96 h avermectin acute toxicity test, and its possible mechanism was discussed. The 96 h LC 50 of avermectin in carp was found to be 24.04 μg/L. Therefore, 3.005 μg/L and 12.02 μg/L were used as the low-dose and high-dose groups, respectively, to investigate the neurotoxic effects of avermectin on carp. The results of high-performance liquid chromatography (HPLC) analysis showed that avermectin accumulated in the carp brain. Histopathological observation and immunohistochemical analysis (IHC) of TNF-α and Bax showed that avermectin exposure led to inflammatory cell infiltration and neuronal necrosis. The mRNA levels of tight junction genes and the IHC results of ZO-1 and Occludin showed that the structure of the blood-brain barrier (BBB) was destroyed. Biochemical analysis showed that avermectin induced the accumulation of MDA in the brain and decreased the activity of antioxidant enzymes CAT and SOD, leading to oxidative stress. In addition, avermectin induces brain inflammation by activating NF-κB pathway and releasing inflammatory factors IL-1β, IL-6, TNF-α and iNOS. TEM and TUNEL assays showed that exposure to avermectin induced apoptosis in brain. what is more, the expression of apoptosis-related genes and proteins suggested that avermectin-induced apoptosis may be associated with inhibition of the PI3K/Akt signaling pathway. This study also showed that avermectin-induced NF-κB signaling activation was partially dependent on its upstream PI3K/Akt signaling pathway. Therefore, this study concludes that avermectin can induce neurotoxicity in carp by disrupting the blood-brain barrier structure and generating oxidative stress, inflammation, and apoptosis and that NF-κB and PI3K/Akt signaling pathways are involved in this process.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMISTRY & BIODIVERSITY
·
2022
·Vol. 19
·期 8
·e202200471
·
IF 2.745
Qiang-Ming Li,Xiu-Rong Yang,Xue-Qiang Zha,Li-Hua Pan,Dan-Dan Zang,Feng-Yun Zhang,Jian-Ping Luo
Dendrobium huoshanense flowers have been widely used for liver protection in China. This work was aimed to discover the natural products with activity of mitigating alcoholic hepatocyte injury from Dendrobium huoshanense flowers via bioactivity-guided isolation, and to clarify the underlying mechanisms of these natural products. As a result, three flavonoids, 3′- O- methylquercetin-3- O-β -D-galactopyranoside ( 1 ), 3′- O- methylquercetin-3- O-β -D-glucopyranoside ( 2 ) and quercetin-3- O-β -D-glucopyranoside ( 3 ), were firstly isolated from D. huoshanense flowers. Results exhibited that flavonoids 1 – 3 could enhance the cell viability, decrease the expression of ALT and AST, inhibit the cell apoptosis, alleviate the oxidative stress, and mitigate the inflammatory response of alcohol-induced L02 cells. Mechanism study exhibited that flavonoids 1 – 3 could increase the expression of Nrf2 as well as its downstream antioxidation genes of alcohol-induced L02 cells, while ML-385 (Nrf2 inhibitor) could abolish the inhibitory effects of 1 – 3 on alcohol-induced hepatocyte injury. Flavonoids 1 – 3 could also reduce the phosphorylation levels of I κ B α and NF- κ B p65 of alcohol-induced L02 cells, while SC75741 (NF- κ B inhibitor) could not enhance the inhibitory effects of 1 – 3 on alcohol-induced L02 cells injury. The data above indicated that flavonoids 1 – 3 could inhibit alcohol-induced hepatocyte injury, which might be attributed to alleviating oxidative stress and mitigating inflammatory response by activating Nrf2 and inhibiting NF- κ B pathways.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2022
·
IF 7.129
Nan Liu,Gai Li,Yi Guan,Rui Wang,Zhanfei Ma,Linlin Zhao,Sanqiao Yao
Indium-tin oxide (ITO) was previously found to have a toxic effect on lung tissues, and oxidative stress and the inflammatory response are two important mechanisms of ITO‑induced lung injury. N-acetylcysteine (NAC) has been found to exhibit antioxidant and anti‑inflammatory properties. The current study aimed to evaluate the possible protective effects of NAC against ITO nanoparticle (Nano-ITO)-induced pulmonary alveolar proteinosis (PAP) in adult male Sprague-Dawley rats, especially via modulation of nuclear factor-kappa B (NF-κB) signaling. For this purpose, 50 rats were randomly allocated into five groups (10 rats each) as follows: (1) control group; (2) saline group; (3) NAC (200 mg/kg) group; (4) PAP model group receiving a repeated intratracheal dose of Nano-ITO (6 mg/kg); and (5) PAP model+NF-κB inhibitor (NAC) group pre-treated intraperitoneally with NAC (200 mg/kg) twice per week before the administration of an intratracheal dose of Nano-ITO (6 mg/kg). Rats were then euthanized under anesthesia, and their lungs were removed for histopathological and biochemical investigations. A 6 mg/kg dose of Nano-ITO markedly altered the levels of some oxidative stress biomarkers. The histological examination of Nano-ITO-exposed rats demonstrated diffused alveolar damage that involved PAP, cholesterol crystals, alveolar fibrosis, pulmonary fibrosis, and alveolar emphysema. The immunohistochemical results of Nano-ITO-exposed rats revealed strongly positive NF-κB p65 and inhibitory kappa B kinase (IKK)-β and weakly positive inhibitor of kappa-B subunit alpha (IκB-α) staining reactivity in the nuclei of cells lining the epithelium of the bronchioles and alveoli. Moreover, Nano-ITO activated the NF-κB pathway. However, pre-treatment with NAC significantly attenuated Nano-ITO-evoked alterations in the previously mentioned parameters, highlighting their antioxidant, anti-inflammatory, and anti-apoptotic potential. The results indicated that the degree of pulmonary fibrosis and proteinosis in the NAC‑treated group was improved compared with that in the Nano-ITO-induced PAP model group. The level of malondialdehyde was also decreased overall in the NAC-treated group compared with that in the Nano-ITO-induced model group, indicating that the pulmonary fibrosis degree and oxidation levels were decreased. The present study also demonstrated that NAC increased the activity of antioxidant enzyme superoxide dismutase and total antioxidant capacity, indicating that it could alleviate oxidative stress in the lung tissue of Nano-ITO‑exposed rats. In addition, NAC reduced the production of pro‑inflammatory cytokines interleukin (IL)‑1β, IL‑6, and tumor necrosis factor (TNF)‑α, and increased the levels of anti‑inflammatory factor IL‑10. The current study demonstrated that NAC can effectively attenuate Nano-ITO‑induced lung injury by reducing oxidative damage and the inflammatory response.
✓ 已验证
DOI
PubMed
高影响因子
SEPARATION AND PURIFICATION TECHNOLOGY
·
2022
·
IF 9.136
Yue Zong,Ruijun Zhang,Shanshan Gao,Jiayu Tian
Reducing the thickness of the polyamide (PA) layer has been confirmed as a feasible strategy to improve the permeability of the thin film composite (TFC) nanofiltration (NF) membrane. In this study, a novel interfacial polymerization (IP) approach assisted by the volatilization of n-hexane was proposed to promote the formation of a thinner PA layer, in which a small amount of n-hexane was added onto the substrate membrane after aqueous phase immersion and before the organic phase coating, then the temperature of the substrate membrane together with the water-soluble monomer solution would be decreased due to the volatilization of n-hexane. The infrared thermographies demonstrated that 7.8 μL cm −2 n-hexane dosage was the most efficient, which can sharply decrease the surface temperature from room temperature (25 °C) to 7.9 °C. The TFC membranes prepared at the lower temperature presented much higher permeability. When PIP concentration was 0.3% w/v, TMC concentration was 0.1% w/v and IP reaction time was 40 s, the PA layer formed at this low temperature was smoother and more hydrophilic. Its thickness was reduced from 26.97 nm to 11.98 nm and water permeability was increased by 50% to 36.7 L m −2 h −1 bar −1 while maintaining Na 2 SO 4 rejection of 96.5%.
✓ 已验证
产品关联
DOI
高影响因子
POULTRY SCIENCE
·
2022
·
IF 4.014
Yusong Miao,Dong Niu,Ze Wang,Jian Wang,Zhiyong Wu,Jiaxin Bao,Xiaodi Jin,Rui Li,Muhammad Ishfaq,Jichang Li
ABSTRACT Mycoplasma gallisepticum ( MG ) is an avian pathogen that commonly causes respiratory diseases in poultry. Methylsulfonylmethane ( MSM ) is a sulfur-containing natural compound that could alleviate inflammatory injury through its excellent anti-inflammatory and antioxidant properties. However, it is still unclear whether MSM prevents MG infection. The purpose of this study is to determine whether MSM has mitigative effects on MG-induced inflammatory injury in chicken and chicken like macrophages ( HD11 cells ). In this research, White Leghorn chickens and HD11 cells were used to build the MG-infection model. Besides, the protective effects of MSM against MG infection were evaluated by detecting MG colonization, histopathological changes, oxidative stress and inflammatory injury of trachea, and HD11 cells. The results revealed that MG infection induced inflammatory injury and oxidative stress in trachea and HD11 cells. However, MSM treatment significantly ameliorated oxidative stress, partially alleviated the abnormal morphological changes and reduced MG colonization under MG infection. Moreover, MSM reduced the mRNA expression of proinflammatory cytokines-related genes and decreased the number of death cells under MG infection. Importantly, the protective effects of MSM were associated with suppression of nuclear factor-kappa B ( NF-κB ) and extracellular signal-related kinases (ERK) /Jun amino terminal kinases (JNK) -mitogen-activated protein kinases ( MAPK ) pathway in trachea and HD11 cells. These results proved that MSM has protective effects on MG-induced inflammation in chicken, and supplied a better strategy for the protective intervention of this disease.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Oleo Science
·
2022
·
IF 1.628
Runzhou Sun,Ruixin Xiao,Pengfei Lv,Feifei Guo,Yanling Gong,Meixing Yan
Pink lotus essential oil (PLEO) is the volatile components extracted from lotus flowers and there are few relevant research. The purpose of this study was to observe the effect of PLEO on NAFLD in vitro model and its possible mechanism. The ingredients of PLEO were determined by gas chromatography-mass spectrometry (GS-MS) and its lipid-lowering and hepatoprotective activities were investigated. HepG2 cells were treated with free fatty acid (FFA) to establish a cell model of NAFLD. Cell viability was evaluated by 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) method. Total cholesterol (TC), triglyceride (TG), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were determined by Enzyme-Linked Immune Sorbent Assay (ELISA). Oil red O staining was performed to observe the lipid accumulation in the HepG2 cells. Lipid metabolism enzymes including fatty acid synthase (FAS), acetyl-coA carboxylase (ACC), stearoyl-CoA desaturase 1 (SCD-1), and carnitine palmitoyltransferase-1 (CPT-1), insulin signaling pathways including phosphatidylinositol 3 kinase (PI3K) and protein kinase B Akt, inflammatory signaling pathways such as nuclear factor kappa-B (NF-κB), were determined by Western blotting. There were 46 components determined in PLEO with many terpenoids compounds. PLEO decreased TC and TG contents in the FFA-treated HepG2 cells. Furthermore, PLEO inhibited TNF-α, IL-6 and IL-1β excretion, decreased NF-κB, FAS, ACC and SCD-1 while increased phosphorylation of NF-κB, PI3K, Akt, and CPT-1 expression. It is the first time to reveal that PLEO alleviates FFA-induced steatosis in HepG2 cells by regulating lipid metabolism, inhibiting inflammatory response, and improving insulin sensitivity.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Oncology Letters
·
2023
·Vol. 25
·期 6
·1-12
·
IF 2.9
Boya Deng,Ailin Li,Ying Zhu,Yingying Zhou,Jing Fei,Yuan Miao
Cervical cancer (CC) is the most common human papillomavirus‑related disease. Continuous activation of the NF‑κB signaling pathway has been observed in CC. SHC binding and spindle associated 1 (SHCBP1) contributes to tumorigenesis and activation of the NF‑κB pathway in multiple cancer types, while its function in CC remains unclear. In the present study, three Gene Expression Omnibus datasets were used to identify differentially expressed genes (DEGs) in CC. Loss‑ and gain‑of‑function experiments were performed using stable SHCBP1‑silenced and SHCBP1‑overexpressing CC cells. To further explore the molecular mechanism of SHCBP1 in CC, small interfering RNA targeting eukaryotic translation initiation factor 5A (EIF5A) was transfected into stable SHCBP1‑overexpressing CC cells. The results demonstrated that SHCBP1 was an upregulated DEG in CC tissues compared with healthy control cervical tissues. Functional experiments revealed the pro‑proliferative and pro‑stemness role of SHCBP1 in CC cells (CaSki and SiHa cells), in vitro. Furthermore, the NF‑κB signaling pathway in CC cells was activated by SHCBP1. Increases in cell proliferation, stemness and activation of NF‑κB, induced by SHCBP1 overexpression in CC cells, were reversed by EIF5A knockdown. Taken together, the results indicated that SHCBP1 serves an important role in regulation of CC cell proliferation, self‑renewal and activation of NF‑κB via EIF5A. The present study demonstrated a potential molecular mechanism underlying the progression of CC.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMISTRY & BIODIVERSITY
·
2026
·Vol. 23
·期 9
·e71695
·
IF 2.9
Li Yang,Junhui He,Dongmei Li,Yi Li,Qibiao Su,Hongning Liang,Jiantong Yuan,Kedao lai,Guining Wei
Water extract of Semiliquidambar cathayensis (WESC) exhibits favorable therapeutic effects against depression, yet its pharmacodynamic material basis and mechanism of action remain unclear. In this study, ultra‐high‐performance liquid chromatography coupled with quadrupole time‐of‐flight mass spectrometry (UPLC‐Q‐TOF‐MS) was employed to analyze the chemical constituents of WESC. Network pharmacology and molecular docking were further applied to screen the antidepressant mechanism basis and potential targets of WESC. Lipopolysaccharide (LPS)‐induced mouse and PC12 cell models were established as in vivo depressive animal model and in vitro cellular injury model, respectively. Combined with pathological examination and molecular biological techniques, the antidepressant mechanism of WESC was systematically investigated. Results showed that a total of 14 chemical components were identified from WESC. Network pharmacology and molecular docking analyses indicated that GSK3β was one of the key targets, and the active components in WESC possessed strong binding affinities with GSK3β, Axin1, and NF‐κB. Pathological studies demonstrated that WESC significantly alleviated inflammatory infiltration in the mouse prefrontal cortex and hippocampal neuronal damage. Molecular biological analyses revealed that WESC markedly downregulated the expression of proteins related to the GSK3β/NF‐κB signaling pathway in LPS‐stimulated mice and PC12 cells, thereby attenuating neuroinflammation, promoting neural plasticity, and exerting antidepressant effects. Ultra‐high‐performance liquid chromatography coupled with quadrupole time‐of‐flight mass spectrometry (UPLC‐Q‐TOF‐MS) was used to characterize the chemical constituents of the water extract of Semiliquidambar cathayensis (WESC). Network pharmacology and molecular docking were applied to screen core active components and potential targets. An LPS‐induced mouse depression model and PC12 cell injury model were established. Combined with HE staining, Western blot, and qRT‐PCR, in vivo and in vitro experiments were carried out to explore the antidepressant mechanism of WESC via regulating signaling pathways and alleviating neuroinflammation.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2026
·
IF 5.6
Chao Zhang,Huai Lan,Liming Yu,Jikai Zhao,Tao Huang,Boxuan Sun,Shan Meng,Jinfeng Duan,Jing Liu,Zijun Zhou,Zhishang Wang,Jiahui Li,Xinyi Huang,Huishan Wang
First to report that radiation-induced atrial fibrillation is driven by cellular senescence. • The GATA4-NF-κB-SASP axis is the key signaling pathway mediating this process. • Senolytic therapy with D/Q (Dasatinib+Quercetin) rescues atrial remodeling and reduces AF susceptibility. • Targeting senescence with senolytics offers a promising strategy to prevent radiation-induced AF. Radiation-induced heart disease is a well-recognized complication of thoracic radiotherapy, with atrial fibrillation (AF) being a particularly notable sequela. The mechanisms by which ionizing radiation (IR) heightens susceptibility to AF remain inadequately understood. This study seeks to elucidate the role of cellular senescence and the GATA4-NF-κB signaling pathway in radiation-induced atrial remodeling and the pathogenesis of AF. An in vivo mouse model was developed through localized cardiac irradiation using 20 Gy X-rays. The irradiated mice demonstrated dose-dependent atrial structural and electrophysiological remodeling. Transcriptomic analysis revealed significant enrichment in DNA damage response (DDR), NF-κB signaling, and aging-related pathways. IR exposure induced substantial DNA damage, activated ATM/ATR pathways, and enhanced autophagic flux. These responses culminated in the accumulation of GATA4 and phosphorylation of NF-κB, which drove the expression of the senescence-associated secretory phenotype (SASP), coinciding with increased senescence-associated β-galactosidase (SA-β-gal) activity. In vitro , these crucial findings were recapitulated using irradiated HL-1 atrial cardiomyocytes, whereas the knockdown of GATA4 effectively suppressed both cellular senescence and SASP expression. Notably, treatment with the senolytic combination of dasatinib and quercetin (D/Q) alleviated DNA damage, inhibited excessive autophagy, and suppressed the GATA4-NF-κB pathway in irradiated mice, thereby reducing SASP levels. These improvements resulted in the reversal of atrial structural and electrophysiological remodeling and a marked reduced susceptibility to AF. Overall, our findings demonstrate that IR promotes atrial remodeling by inducing DNA damage-mediated cellular senescence via the GATA4-NF-κB-SASP axis. Targeting this pathway with senolytics such as D/Q thus identifies a promising therapeutic strategy for preventing radiation-induced atrial fibrillation.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
·
2023
·
IF 4.7
Haoye Li,Qingwen Yang,Haitong Wu,Jianying Guo,Zhaoxin Tang,Jianzhao Liao
Terbuthylazine (TBA), a triazine herbicide, is extensively employed in agriculture for its wide range of effectiveness. However, prolonged utilization of TBA can pose a potential hazard to animals and human health. Here, a total of 180 broiler chickens ( Gallus gallus ) were stochastically assigned to three groups (control group, 0.4 mg/kg TBA group, and 4 mg/kg TBA group) for investigating the impact of TBA on cardiotoxicity. The results revealed that TBA exposure resulted in pathological alterations in the myocardium . Moreover, TBA exposure activated cGAS-STING pathway and markedly elevated the mRNA and protein expression levels of innate immune response (cGAS, STING, TBK1, and IRF3) in myocardium. Additionally, NF-κB signal was also activated under TBA exposure, which was characterized by the increasing mRNA expression levels of NF-κB, IKKα and the protein expression levels of p-NF-κB/NF-κB, IKKα, p-IκBα/IκBα in the TBA treatment groups. Meanwhile, the expression of pro-inflammatory cytokines (TNF-α and IL-1β) were also significantly increased. In summary, our findings suggested that cGAS-STING/NF-κB pathway functionated in the innate immune response and inflammation in myocardium brought on by TBA exposure, which provided new insights into the TBA toxicology.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Journal of Oleo Science
·
2023
·
IF 1.5
Ting Wu,Yueqing Xie,Zhikai Wu,Yifei Li,Mingzhen Jiang,Hongsen Yu,Xuhai Li,Jingjing Wang,Ershun Zhou,Zhengtao Yang
Acute liver injury (ALI), posing a serious threaten to our life, has emerged as a public health issue around the world. β-carotene has plenty of pharmacologic effects, such as anti-inflammatory, antioxidant, and antitumor activities. In this study, we focused on studying the protective role and potential molecular mechanisms of β-carotene against D-galactosamine (D-GalN) and lipopolysaccharide (LPS) induced ALI. Our results indicated that β-carotene pretreatment effectively hindered abnormal changes induced by LPS/D-GalN in liver histopathology. Meanwhile, serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were downgraded with β-carotene pretreatment. β-carotene pretreatment also decreased malondialdehyde content and myeloperoxidase activity, increased glutathione peroxidase and superoxide dismutase levels, and reduced the levels of tumor necrosis factor-a (TNF-α) and interleukin 6 (IL-6) in liver tissues. Further investigations found that β-carotene mediated multiple signaling pathways in LPS/D-GalN-induced ALI, inhibiting NF-κB and MAPK signaling and upregulating the expression of Nrf2 and HO-1 proteins. All findings indicate that β-carotene appears to protect mice against LPS/D-GalN induced ALI by reducing oxidative stress and inflammation, possibly via regulating NF-κB, MAPK, and Nrf2 signaling.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MOLECULAR IMMUNOLOGY
·
2023
·
IF 3.6
Zhijun Zhao,Yongqing Tong,Yuting Kang,Zhuoran Qiu,Qiujie Li,Chao Xu,Geng Wu,Wei Jia,Pengtao Wang
Cigarette smoke is recognized as a major trigger for individuals with chronic obstructive pulmonary disease (COPD), leading to an amplified inflammatory response. The onset and progression of COPD are affected by multiple environmental and genetic risk factors, such as inflammatory mechanisms, oxidative stress, and an imbalance between proteinase and antiprotease. As a result, conventional drug therapies often have limited effectiveness. This study aimed to investigate the anti-inflammatory effect of sodium butyrate (SB) in COPD and explore its molecular mechanism, thereby deepening our understanding of the potential application of SB in the treatment of COPD. In our study, we observed an increase in the mRNA and protein expressions of inflammatory factors interleukin-1beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), Matrix metallopeptidase 9 (MMP9) and MMP12 in both NR8383 cell and rat models of COPD. However, these expressions were significantly reduced after SB treatment. Meanwhile, SB treatment effectively decreased the phosphorylation levels of nuclear transcription factor-kappa B (NF-κB) p65, c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) and inhibited the nuclear translocation of these proteins in the COPD cells, leading to a reduction in the expression of various inflammatory cytokines. Additionally, SB also inhibited the expression level of the Nod-like receptor pyrin domain 3 (NLRP3) inflammasome, which consists of NLRP3, apoptosis-associated speck-like protein (ASC), and Caspase-1 in the cigeratte smoke extract (CSE)-stimulated cells. Our results showed that CSE down-regulated the mRNA levels of G-protein-coupled receptor 43 (GPR43) and GPR109A, while SB only up-regulated the expression of GPR43 and had no effect on GPR109A. Moreover, additional analysis demonstrated that the knockdown of GPR43 diminishes the anti-inflammatory effects of SB. It is evident that siRNA-mediated knockdown of GPR43 prevented the reduction in mRNA expression of IL-1β, IL-6, TNF-α, MMP9, and MMP12, as well as the expression of phosphorylated proteins NF-κB p65, JNK, and p38 MAPKs with SB treatment. These findings revealed a SB/GPR43 mediated pathway essential for attenuating pulmonary inflammatory responses in COPD, which may offer potential new treatments for COPD.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）