AQUACULTURE
·
2022
·
IF 5.135
Min Li,Xueqin Wu,Jixing Zou,Yingqian Lai,Jiawen Zhang,Xiumei Chen,Xiaotian Niu,Yidi Kong,Guiqin Wang
This study was aimed to evaluate the ameliorative effects of thymol-supplemented diets on the toxicity damage of Channa argus induced by deltamethrin (DEL). After 28 d, the results are as follows: thymol can attenuate DEL-induced oxidative stress by reversing the decrease of the activities of antioxidant enzyme (SOD, CAT , GSH , GST and GSH-Px) and the increase of the MDA content in the tissues (liver and spleen), and also by reversing the decrease of the mRNA expression levels of Nrf2, Cu/Zn SOD and HO-1, and the increase of the Keap1 mRNA expression level in the tissues (liver and spleen). Thymol can attenuate DEL-induced immunotoxicity of fish by reverse the decrease of the levels of humoral immune parameters (C4, C3, IgM and LYS) in the serum, and by reversing the increase of the expression levels of NF-κB p65, TNF-α, IL-1β, IL-8 and IL-6, and the decrease of the IL-10 expression level in the tissues (liver and spleen). Thymol can attenuate DEL-caused apoptosis reversing the increase of the expression levels of pro-apoptosis (p53, Bax and Apaf-1) and the decrease of the expression level of anti-apoptosis Bcl-2 in the tissues (liver and spleen). Therefore, this study reveals that dietary supplementation of thymol alleviates DEL-caused immunotoxicity, oxidative stress, and apoptosis of C. argus in association with the NF-κB/Nrf2/p53 pathway.
✓ 已验证
产品关联
DOI
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2022
·
IF 5.895
Sen Li,Yu Chen,Yu Zhang,Hongyan Lv,Lei Luo,Shuo Wang,Xiao Guan
Coffee cherry husks, the main byproduct of coffee production, contain an abundance of polyphenols. In this study, dextran sodium sulfate (DSS)-induced colitis mice were used to study the protective effects of polyphenolic extracts of coffee cherry husks (CCHP) on inflammation. The results indicated that CCHP administration alleviated the histological changes of DSS-induced colitis in mice and downregulated the mRNA level of TNF-α, IL-1β, IL-6 and Cox-2. Interestingly, CCHP inhibited the activation of microglia and suppressed neural inflammation in the brain. The TLR4/Myd88/NF-κB signaling pathway was examined and found to be inhibited by CCHP. Furthermore, a determination of the gut microbiota showed that an alteration of microbiota induced by DSS was restored by CCHP, including the decrease of the relative abundance of Proteobacteria and the increase of Bacteroidota. In conclusion, our results revealed the great potential of CCHP to alleviate brain inflammation in colitis mice by inhibiting the NF-κB signaling pathway and regulating gut microbiota.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMICAL & PHARMACEUTICAL BULLETIN
·
2022
·Vol. 70
·期 1
·66-73
·
IF 1.903
Li Han,Aimei Chen,Ling Liu,Fang Wang
Despite the precise mechanisms for renal ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) are poorly understood, nuclear factor erythroid 2 related factor 2 (Nrf2) and Toll-like receptor 4 (TLR4) pathways were considered as the important targets. Leonurine (LEO) is a special alkaloid extracted from Chinese motherwort (Leonurus japonicus Houtt), which has an anti-inflammatory effect and reduces oxidative stress. We conducted the study to explore the efficacy of LEO against I/R-induced AKI in rats and further investigated the underlying mechanisms. Ischemic renal injury was induced by temporary vascular clamping for 45 min. We have measured the levels of inflammation-related biomarkers and antioxidative stress markers. Next, Western blot analysis and Real-time PCR were performed to analyze whether the Nrf2 and TLR4/nuclear factor-kappaB (NF-κB) pathways were involved in this process. We found that LEO pretreatment remarkably decreased serum creatinine and blood urea nitrogen (BUN) in I/R rats and attenuated acute tubular damage. In addition, LEO markedly increased the expression of antioxidant proteins and decreased the levels of inflammatory factors. Further study revealed that LEO promoted Nrf2 into the nucleus, promoted the expression of heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1), and suppressed the TLR4/NF-κB signal pathway in kidney tissues of ischemic AKI rats. The study reveals that LEO has a protective effect to prevent ischemic AKI through activation of Nrf2 nuclear translocation resisting oxidative stress injury and inhibition of the TLR4/NF-κB pathway mediated inflammatory gene expression.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ELECTROANALYTICAL CHEMISTRY
·
2021
·
IF 4.464
Ruili Zhang,Tian Fang,Liping Ni,Yaping Zhu,Yuhua Shen,Anjian Xie,Li Lao
So far, the high theoretical specific capacity metal oxide is considered as a promising anode material for lithium-ion batteries (LIBs). Unfortunately, the intrinsic poor conductivity and structural stability of metal oxide, the huge volume expansion during the cycling cause serious capacity fading and unstable cycle. Here, the three-dimensional (3D) ordered inverse opal (IO) heterojunction structure of SnO 2 /Bi 2 O 3 on commercial nickel foam (NF) were fabricated. When used as a binder-free anode material for LIBs, the initial discharge specific capacity and charge specific capacity of the IOs electrode were 1229 mA h g −1 and 1098 mA h g −1 . The SnO 2 /Bi 2 O 3 /NF IOs exhibited excellent electrochemical activity and delivered a discharge capacity about 493 mA h g −1 after 500 cycles at the current density of 1000 mA g −1 , the Coulomb efficiency (CE) had been maintained at around 100%, which was much more than the control groups of SnO 2 /NF IOs (247 mA h g −1 ) and Bi 2 O 3 /NF IOs (124 mA h g −1 ). Furthermore, the prepared was successfully assembled with commercial LiFePO 4 to a full cell that displayed stable capacity about 101.2 mA h g −1 at the current density of 100 mA g −1 after 100 cycles. The excellent performance of SnO 2 /Bi 2 O 3 /NF IOs is due to that the 3D interconnected macroporous and mesoporous structures can shorten the transmission path of ions/electrons and buffer volume expansion. In addition, the heterojunction structure with obvious lattice defects can effectively promote the contact between electrode material and electrolyte. The strategy in this study lights on the illuminating design of 3D inverse opal heterostructure binder-free anode, and the obtained product has a great potential as the anode material applied in next-generation LIBs.
✓ 已验证
产品关联
DOI
高影响因子
Microorganisms
·
2021
·Vol. 9
·期 9
·1983
·
IF 4.128
Shiyan Chen,Yanan Li,Bingxin Chu,Lanxin Yuan,Ning Liu,Yaohong Zhu,Jiufeng Wang
SalmonellaTyphimurium (S.Typhimurium) is an aggressive zoonotic pathogen that causes enteritis and diarrhea. Antibiotic therapy is still the primary method at present. However, the increasing emergence of multi-drug resistant bacteria weakens the therapeutic efficacy of antibiotics. Probiotics have been widely studied as an alternative antibiotic therapy. In this study, we established an IPEC-J2 cell model ofS.Typhimurium infection, aiming to determine the protective effect ofLactobacillus johnsoniiL531 (L. johnsoniiL531) onS.Typhimurium infection. As our data showed,S.Typhimurium infection resulted in a robust inflammatory response demonstrated by promoted protein levels of the inflammatory-related pathway (TLR4, MyD88, p-IκBα, and p-p65), increased cytokine levels of IL-6, IL-1β, IL-18, and TNF-α, and activated the NLRP3 inflammasome via promoting its assembly. However,L. johnsoniiL531 pre-incubation inhibited the activation of the above inflammatory signaling pathways and reduced the expression levels of pro-inflammatory cytokines. In addition,L. johnsoniiL531 alleviated the damage ofS.Typhimurium to tight junctions ZO-1, Occludin, and Claudin-1. In summary, our findings suggested thatL. johnsoniiL531 alleviatedS.Typhimurium-induced tight junction injury by inhibiting the TLR4/NF-κB/NLRP3 inflammasome signaling pathway.Keywords:SalmonellaTyphimurium;Lactobacillus johnsonii;TLR4;NF-κB;NLRP3 inflammasome;tight junctions
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ELECTROANALYTICAL CHEMISTRY
·
2021
·
IF 4.464
Xiaoyu Ma,Shihong Zhang,Yi He,Teng He,Hongjie Li,Yihan Zhang,Jingyu Chen
Developing highly efficient, inexpensive, and stable electrocatalysts for hydrogen evolution reaction (HER) is indispensable to building a sustainable and large-scale hydrogen conversion system. In this work, we designed a ternary NiVFe layered double hydroxide nanosheet on porous nickel foam via hydrothermal method to prepare a self-supporting electrocatalyst and co-doped with boron and phosphorus which control the electronic structure of the nanosheets. Simultaneous, the B-P co-doping formation numerous defects and amorphous regions on the nanosheet, which guarantees efficient active sites and enhanced active surface area. As expected, the electrochemical test of HER results shows that the NiVFe-B-P LDHs@NF requires an overpotentials of 117 mV at a current density of 10 mA·cm −2 in the 1.0 M KOH electrolyte without iR compensation, as well as exhibits excellent stability of 24 h at current densities of 10 mA·cm −2 and 50 mA·cm −2 , respectively. Moreover, evaluation of wettability shows that the electrocatalyst has excellent superhydrophilicity and superaerophobicity. We expect the results of this work provides a fresh perspective for double-nonmetal co-doping electrocatalysts with efficient hydrogen generation.
✓ 已验证
产品关联
DOI
高影响因子
INFLAMMATION
·
2021
·Vol. 44
·期 5
·2018-2032
·
IF 4.092
Zhou Changkai,Gao Jing,Ji Hongyan,Li Wenjing,Xing Xiaomin,Liu Donghua,Guo Qie,Zhou Lihua,Jing Fanbo
Previous studies have shown that benzoylaconine (BAC), a representative monoester alkaloid, has a potential anti-inflammatory effect. This study investigated the underlying molecular mechanisms using the mode of LPS-activated RAW264.7 macrophage cells. Our findings showed that BAC significantly suppressed the release of pro-inflammatory cytokines and mediators, including IL-6, TNF-α, IL-1β, ROS, NO, and PGE 2 . BAC treatment also effectively downregulated the elevated protein levels of iNOS and COX-2 induced by LPS in a dose-dependent manner. In this study, we found that BAC inhibited LPS-induced NF-κB activation by reducing the phosphorylation and degradation of IκBα by western blotting and blocking the nuclear translocation of p65 using an immunofluorescence assay. The elevated protein levels of JNK, p38, and ERK phosphorylation after LPS stimulation were restored effectively by BAC treatment. The protein expression of Toll-like receptor 4 (TLR4) and LPS-induced phosphorylation of TAK1, which is a crucial upstream regulatory factor of TLR-induced MAPK and NF-κB signaling, were inhibited by BAC in activated RAW264.7 macrophages. Moreover, BAC decreased the levels of TAK1 phosphorylation and pro-inflammatory cytokines and mediators associated with MAPK and NF-κB activation, similar to TLR4 inhibitor TAK-242. These findings demonstrated that BAC exhibited an anti-inflammatory effect by the inhibition of TLR-induced MAPK and NF-κB pathways, indicating that it could potentially be used for treating inflammatory diseases.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF BIOCHEMISTRY
·
2021
·Vol. 170
·期 3
·349-362
·
IF 3.387
Liu Xiaoyu,Guo Bingyan,Zhang Wei,Ma Bocong,Li Yongjun
Diabetic cardiomyopathy (DCM) is a common cardiovascular disease. A declined miR-20a-5p was observed in hearts of diabetic mice, while its effect on DCM remains unknown. Herein, we established streptozotocin-induced DCM rat model and high glucose-stimulated H9C2 model of DCM. Then they were treated with adenovirus expressing miR-20a-5p to explore the function of miR-20a-5p. Insulin tolerance test and intraperitoneal glucose tolerance test assay revealed that miR-20a-5p reduced blood glucose level. Besides, miR-20a-5p improved cardiac dysfunction reflected by reduced heart weight/body weight and left ventricular diastolic pressure, and increased left ventricular systolic pressure and ±LV dp/dt max. MiR-20a-5p prevented cardiomyocyte apoptosis, along with the upregulated c-caspase-3, bax and downregulated bcl-2. Moreover, miR-20a-5p alleviated cardiac hypertrophy as the parameters of atrial natriuretic peptide, B-type natriuretic peptide and MyHC-β decreased. Also, miR-20a-5p attenuated the cardiac fibrosis demonstrated by decreased transforming growth factor-β1, collagen I levels and the inflammatory response manifested by reduced interleukin-6, tumour necrosis factor-α and IL-1β production. Furthermore, miR-20a-5p prevented Jun NH2-terminal kinase (JNK) phosphorylation and nuclear factor-κB (NF-κB) p65nuclear translocation. Similarly, the effects of miR-20a-5p on DCM were confirmed in our in vitro experiments. Additionally, ROCK2 is a possible target gene of miR-20a-5p. ROCK2 overexpression reversed the protective effect of miR-20a-5p on DCM. Overall, miR-20a-5p may effectively ameliorate DCM through improving cardiac metabolism, and subsequently inhibiting inflammation, apoptosis, hypertrophy, fibrosis and JNK/NF-κB pathway via modulating ROCK2.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Frontiers in Oncology
·
2021
·
IF 6.244
Heng Yongqing,Liang Yupei,Zhang Junqian,Li Lihui,Zhang Wenjuan,Jiang Yanyu,Wang Shiwen,Jia Lijun
The neddylation pathway is overactivated in esophageal cancer. Our previous studies indicated that inactivation of neddylation by the NAE inhibitor induced apoptosis and autophagy in cancer cells. Camptothecin (CPT), a well-known anticancer agent, could induce apoptosis and autophagy in cancer cells. However, whether CPT could affect the neddylation pathway and the molecular mechanisms of CPT-induced autophagy in esophageal cancer remains elusive. We found that CPT induced apoptosis and autophagy in esophageal cancer. Mechanistically, CPT inhibited the activity of neddylation and induced the accumulation of p-IkBa to block NF-κB pathway. Furthermore, CPT induced the generation of ROS to modulate the AMPK/mTOR/ULK1 axis to finally promote protective autophagy. In our study, we elucidate a novel mechanism of the NF-κB/AMPK/mTOR/ULK1 pathway in CPT-induced protective autophagy in esophageal cancer cells, which provides a sound rationale for combinational anti-ESCC therapy with CPT and inhibition AMPK/ULK1 pathway.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2021
·
IF 5.279
Jinwen Yuan,Siyan Che,Li Zhang,Zheng Ruan
Luteolin, a dietary flavonoid, has gained increasing interest as an intestinal protectant. This study aimed to evaluate the reparative effect of luteolin against ethanol-induced intestinal barrier damage in a Caco-2 cell monolayer model and the potential mechanisms. Luteolin attenuated ethanol-induced intestinal barrier injury, by increasing transepithelial monolayer resistance (TEER, 27.75 ± 14.75% of the ethanol group, p < 0.01), reducing Lucifer yellow flux (13.21 ± 1.23% of ethanol group, p < 0.01), and upregulating the expression of tight junction (TJ) proteins zonulin occludin-1 (ZO-1), occludin, and claudin-1 (37.963 ± 8.62%, 17.69 ± 7.35%, and 29.40 ± 8.08% of the ethanol group, respectively, p < 0.01). Further mechanistic studies showed that luteolin suppressed myosin light chain 2 (MLC) phosphorylation, myosin light chain kinase (MLCK) activation, nuclear factor kappa-B (NF-κB) nuclear translocation, and mitogen-activated-protein-kinase (MAPK) phosphorylation. Moreover, luteolin also acted as antioxidants indirectly by upregulating antioxidant-responsive-element (ARE) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation to relieve ethanol-induced oxidative damage and TJ dysfunction. The results of the study indicate that luteolin may play an effective role in relieving intestinal barrier damage, and this effect is at least partially due to its indirect antioxidant capacity.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
PULMONARY PHARMACOLOGY & THERAPEUTICS
·
2021
·
IF 3.41
Bo Zou,Yue Fu,Chaofan Cao,Dianzhu Pan,Wei Wang,Lingfei Kong
Allergic asthma is a common airway inflammatory disorder with increasing morbidity and mortality worldwide. Gentiopicroside (GPS) is a secoiridoid glycoside compound that exhibits anti-inflammatory property. However, the effect of GPS on allergic asthma has not been reported yet. In this study, we investigated the role of GPS in a mouse model of ovalbumin (OVA)-induced allergic asthma and explored its potential mechanism. Mice were sensitized with OVA and gavaged with 20, 40, or 80 mg/kg GPS. Administration of GPS decreased lung wet-to-dry weight ratio. Histological analysis of H&E and PAS staining showed that GPS treatment alleviated inflammatory cell infiltration and goblet cell hyperplasia in lung tissue of OVA-sensitized mice. Moreover, GPS inhibited the recruitment of inflammatory cells including total cells, macrophages, eosinophils , lymphocytes and neutrophils and the secretion of T helper type 2 (Th2) cytokines (interleukin (IL)-4, IL-5 and IL-13) in bronchoalveolar lavage fluid (BALF) of OVA-sensitized mice in a dose dependent manner. The levels of OVA-specific immunoglobulin E (IgE) and pro-inflammatory tumor necrosis factor (TNF)-α were also attenuated by GPS treatment. Interestingly, GPS upregulated the expression of silent information regulator 1 (SIRT1) while downregulated the expression of acetyl-nuclear factor kappa B (NF-κB) p65 in lung tissue of OVA-sensitized mice. Furthermore, treatment with an SIRT1 inhibitor (EX-527) partially abolished the inhibitory effect of GPS on OVA-induced airway inflammation, suggesting that the anti-inflammation of GPS might be achieved through regulating SIRT1/NF-κB p65 signaling pathway . These findings indicate that GPS might be a novel drug candidate in the treatment of allergic asthma.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2020
·
IF 3.347
Qiongtao Song,Ying Zhao,Yanrong Yang,Xue Han,Junguo Duan
Iron overload toxicity has been implicated in retinal pigment epithelial cell injury in age-related macular degeneration. This study investigates the effects of astragaloside IV (AS-IV), a potential retinal protective agent, on the toxicity process of retinal iron overload in vivo and in vitro . AS-IV partially restored the retinal expression of rhodopsin and retinal pigment epithelium-specific 65 kDa protein, suppressed oxidative stress and inflammatory markers, and alleviated iron deposition and retinal pathological changes in vivo . Also, AS-IV inhibited the phosphorylation of p38 and ERK mitogen-activated protein kinases (MAPKs), as well as the nuclear translocation of nuclear factor-kappa B (NF-κB). Furthermore, AS-IV prevented cell death by decreasing the ratio of Bax/Bcl-2, caspase-3, and cleaved caspase-3 expression in vitro . Although there are no chelation effects between AS-IV and iron, AS-IV can reduce intracellular iron by regulating iron-handling proteins in ARPE-19 cells (Cav1.2, divalent metal transporter-1, transferrin receptor 1 , and heavy-chain ferritin). In conclusion, the results show that AS-IV has significant protective effects against retinal iron overload toxicity and suggest that iron regulation and the inhibition of MAPKs and NF-κB activation might be mechanisms underlying the effects of AS-IV.
✓ 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）