APPLIED CATALYSIS B-ENVIRONMENTAL
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2025
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IF 21.1
Xiao Chen,Yating Hou,Jinghan Xu,Ningyuan Song,Xinru Wei,Yanru Liu,Kang Liu,Yunmei Du,Lei Wang
Nowadays, the electrocatalytic regulation mechanism of quantum dots (QDs)-supported materials is limited to strong metal-support interaction (SMSI) and electron-metal-support interaction (EMSI). However, the lattice strain of the carrier induced by QDs is neglected, which is not conducive to the directional design of the QDs-supported electrode and the establishment of its structure-performance correlation. Given these, the size and distribution of Pt QDs controlled by electrodeposition effectively regulate the strain degree on S-NiFeP nanosheets. DFT results reveal that Pt@S-NiFeP/NF complies with a Fe-Pt dual active sites mechanism for alkaline HER, and a Fe active site mechanism for OER. Interestingly, the compressive strain in the S-NiFeP substrate effectively promotes the d‐band center shift and the energy barrier reduction, thereby optimizing the alkaline HER and OER kinetics. As expected, Pt@S-NiFeP/NF with appropriate strain owns alkaline HER and OER performance at 1 A cm −2 that exceeds the commercial Pt/C and RuO 2 . Overall, this work has guided the structural design of the 'noble metal QDs@carrier' model and laid a foundation for its application at ampere-level current densities.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2025
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IF 6.2
Lei Diao,Yang Ma,Liping Wang,Peng Li,Bin Zhang,Weijing Meng,Jingzeng Cai,Yan Meng,Yuxun Zhou,Jingying Zhai,Huijie Chen
Thiacloprid (THI) is a synthetic insecticide, the misuse is targeted chiefly to control aphid pest species in orchards and vegetables. Melatonin (MET) is a hormone that plays crucial physiological roles in anti-inflammatory capacities of fish. We explored the function of MET (100 μM) to mitigate the toxicity induced by THI (20 μM) in lymphocytes. Our results indicate that THI led to a notable rise in lymphocyte mortality. Lymphocytes exposed to THI exhibited a heightened incidence of pyroptosis, accompanied by upregulation in expression associated with pyroptosis (NLRP3, GSDMEA, and IL-18). Meanwhile, THI exposure led to a decrease in lymphocyte mitochondrial membrane potential, an increase in mtROS levels, and a reduction in intracellular ATP, DNA, and NADPH/NADP+ levels, indicating an imbalance in the mitochondrial metabolism within the lymphocytes. Additionally, these effects were reversed by MET treatment, where MitoQ treatment showed that the suppression of mtROS reduced the lymphocyte pyroptosis caused by THI via the mtROS/cGAS-STING/NF-κB axis. Importantly, MET provided defense against the immunotoxic impacts of THI by ameliorating pyroptosis and enhancing anti-inflammatory capability via the mtROS/cGAS-STING/NF-κB axis. Our research potentiates the safeguarding of cultured fish from biological hazards caused by THI and highlights the valuable application of MET in common carp.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2025
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IF 6.2
Jingjing Wang,Pingping Qu,Fuhan Wang,Man Qian,Ziyi Li,Mengyao Guo,Xuejiao Gao
Zearalenone is an estrogen-like mycotoxin produced by Fusarium fungi. Growing evidence shows that ZEA causes multisystem damage via oxidative stress. Glycyrrhizic acid (GA), from Glycyrrhiza glabra, has anti-inflammatory/antioxidant properties. The mechanisms of GA and ZEA in chicken pulmonary oxidative stress and inflammation remain elusive. Therefore, we established zearalenone-exposed chicken lung and CP-II cells models. ZEA exposure triggers an inflammatory cascade via the ROS-NF-κB axis, activating NLRP3 inflammasomes and promoting the release of proinflammatory factors. It also increased the apoptosis-related factors and fibrosis-related factors. GA treatment reduced oxidative stress, inflammation, and apoptosis, while suppressing fibrosis. This study reveals that GA reverses lung tissue injury by suppressing oxidative stress, inflammation, and the apoptosis-necrosis network through regulating the NF-κB/NLRP3 signaling axis by scavenging ZEA-induced reactive oxygen species (ROS). These results elucidate the antioxidant mechanism of GA and provide insights into the toxicology of ZEA.
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Journal of Functional Foods
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2015
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IF 3.574
Dongli Li,Zhiyun Du,Chenyue Li,Yue Liu,Susan Goodin,Huarong Huang,Yan He,Yuan Zhang,Huaqian Wang,Xi Zheng,Kun Zhang
Five terpenoids ( 1 – 5 ) from a vegetable plant Acanthopanax trifoliatus (L.) Merr. were investigated for their effects on human prostate cancer cells. The diterpenoid ( 3 ) and triterpenoids ( 4 and 5 ) were found to inhibit the growth and stimulate apoptosis in PC-3 cells. The effects of these terpenoids on PC-3 cells were associated with strong suppression of nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3). These terpenoids also inhibited the expression of survivin, a downstream target of NF-κB and STAT3. The in vivo study using a xenograft mouse model showed that 5 strongly inhibited the formation and growth of PC-3 tumours. Moreover, treatment with 5 strongly decreased the expression of phospho-STAT3 and survivin in PC-3 tumours. Our results indicate that 5 has preventive efficacy on the development of PC-3 xenograft tumours. This terpenoid may serve as a candidate for future development as a novel agent for prostate cancer prevention.
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MEDICAL SCIENCE MONITOR
·
2021
·
IF 2.649
Cuizhen Long,Na Xie,Yuanhui Shu,Yafeng Wu,Ping He,Yan Zhou,Yining Xiang,Junying Gu,Lei Yang,Yuping Wang
Background This study aimed to investigate the effect of deleting the cannabinoid receptor 2 (CB2) gene on the development of hepatic fibrosis induced by carbon tetrachloride (CCl 4 ) in mice via regulating inflammation. Material/Methods The DNA was extracted from the tails of mice to identify whether the cannabinoid receptor 2 gene was successfully knocked out. A liver fibrosis model was established by an intraperitoneal injection of CCl 4 into mice. Hepatic damage and hepatic fibrosis were evaluated by detecting serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and staining paraffin sections of liver tissue with hematoxylin-eosin (HE). The secretion and distribution of collagen in liver tissue were observed by Masson staining. Western blot analysis was performed to detect the expression of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), tumor necrosis factor alpha-induced protein 3 (A20), phosphorylated nuclear factor-κB p65 (p-NF-κB p65), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) in liver tissue. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of IL-6 and TNF-α mRNA in liver tissue. Results Compared with the control mice, the mice with CB2 knockout that were exposed to CCl 4 exhibited increased liver damage, liver fibrosis, and upregulated α-SMA, TGF-β1, A20, and p-NF-κB p65 protein levels. IL-6 and TNF-α protein levels and mRNA levels were upregulated. Conclusions The deletion of the CB2 gene promoted the activation of hepatic stellate cells in mice with liver fibrosis and aggravated liver fibrosis by up-regulating the protein expression of A20 and p-NF-κB p65 and inducing inflammatory response, potentially providing new insight into the treatment of liver fibrosis.
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2022
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IF 7.129
Chongshan Dai,Meng Li,Yue Liu,Diem Hong Tran,Haiyang Jiang,Shusheng Tang,Jianzhong Shen
Chronic copper exposure could cause potential nephrotoxicity and effective therapy strategies are limited. This study investigated the protective effects of curcumin on copper sulfate (CuSO 4 )-induced renal damage in a mouse model and the underlying molecular mechanisms. Mice were administrated orally with CuSO 4 (100 mg/kg per day) in combination with or without curcumin (50, 100 or 200 mg/kg per day, orally) for 28 days. Results showed that curcumin supplementation significantly reduce the Cu accumulation in the kidney tissues of mice and improved CuSO 4 -induced renal dysfunction. Furthermore, curcumin supplantation also significantly ameliorated Cu exposure-induced oxidative stress and tubular necrosis in the kidneys of mice. Moreover, compared to the CuSO 4 alone group, curcumin supplementation at 200 mg/kg per day significantly decreased CuSO 4 -induced the expression of p53, Bax, IL-1β, IL-6, and TNF-α proteins, levels of NF-κB mRNA, levels of caspases-9 and − 3 activities, and cell apoptosis, and significantly increased the levels of Nrf2 and HO-1 mRNAs in the kidney tissues. In conclusion, for the first time, our results reveal that curcumin could trigger the inhibition of oxidative stress, mitochondrial apoptotic, p53, and NF-κB pathways and the activation of Nrf2/HO-1 pathway to ameliorate Cu overload-induced nephrotoxicity in a mouse model. Our study highlights that curcumin supplementation may be a promising treatment strategy for treating copper overload-caused nephrotoxicity.
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Heliyon
·
2024
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IF 3.4
Chongchong Liu,Jiangyan Sun,Xiaoming Shen,Shefang Li,Sha Luo,Na Chen,Yunke Zhang
Epilepsy is a chronic neurological disorder. Drug-resistant epilepsy (DRE) accounts for about one-third of epilepsy patients worldwide. Peimine, a main active component of Fritillaria, has been reported to show anti-inflammatory effects. However, its potential therapeutic role in DRE is not yet fully understood. In this work, a DRE rat model was established by injecting 1 μg kainic acid (KA), followed by a 250 mg/kg administration of valproic acid (VPA) from day 4–31. Rats were treated with different doses of peimine (2.5 mg/kg, 5 mg/kg and 10 mg/kg) daily from day 32–62. In vitro, BV-2 microglia were exposed to different doses of peimine (7.5 μg/ml, 15 μg/ml, and 30 μg/ml) in presence of LPS. The aim of this study was to investigate the potential therapeutic effects of peimine on DRE. The results showed that peimine efficiently suppressed the KA-induced epileptic behaviors of rats in a dose-dependent manner, as recorded by electroencephalography. Furthermore, peimine ameliorated hippocampal neuron injury in DRE rats, and promoted an M1-to-M2 microglial phenotype shift in a dose-dependent manner. Mechanistically, peimine inhibited the TLR4/NF-κB/HIF-1α signaling pathway both in vivo and in vitro. Additionally, peimine suppressed the apoptosis of primary neurons induced by LPS-treated microglia. In conclusion, peimine augments the microglial polarization towards an M2 phenotype by inhibiting the TLR4/NF-κB/HIF-1α signaling pathway, thereby attenuating DRE.
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
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2023
·Vol. 24
·期 4
·3575
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IF 5.6
Yangling Chen,Rui Chen,Renyikun Yuan,Lini Huo,Hongwei Gao,Youqiong Zhuo,Xinxin Chen,Chenwei Zhang,Shilin Yang
NF-κB and MAPK are classic inflammation signaling pathways which regulate inflammation signal transmission and induce the expression of many inflammatory factors. Based on the potent anti-inflammatory activity of benzofuran and its derivatives, several new heterocyclic/benzofuran hybrids were first designed and synthesized by molecular hybridization. Their structure was confirmed by1H NMR,13C NMR, HRMS or X-single crystal diffraction. The anti-inflammatory activity of these new compounds was screened by compounds; compound5dexhibited an excellent inhibitory effect on the generation of NO (IC50= 52.23 ± 0.97 μM), and low cytotoxicity (IC50> 80 μM) against the RAW-264.7 cell lines. To further elucidate the possible anti-inflammatory mechanisms of compound5d, the hallmark protein expressions of the NF-κB and MAPK pathways were studied in LPS-stimulated RAW264.7 cells. The results indicate that compound5dnot only significantly inhibits the phosphorylation levels of IKKα/IKKβ, IKβα, P65, ERK, JNK and P38 in the classic MAPK/NF-κB signaling pathway in a dose-dependent manner, but also down-regulates the secretion of pro-inflammatory factors such as NO, COX-2, TNF-α and IL-6. Further, the in vivo anti-inflammatory activity of compound5dindicated that it could regulate the involvement of neutrophils, leukocytes and lymphocytes in inflammation processes, and reduce the expression of IL-1β, TNF-α and IL-6 in serum and tissues. These results strongly suggest that the piperazine/benzofuran hybrid5dhas a good potential for developing an anti-inflammatory lead compound, and the anti-inflammatory mechanism might be related to the NF-κB and MAPK signaling pathways.Keywords:benzofuran derivatives;piperazine;anti-inflammatory;NF-κB/MAPK signaling pathway;endotoxemic mice
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INTERNATIONAL IMMUNOPHARMACOLOGY
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2017
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IF 2.956
Zhaoxiao Yu,Chenhui Zhang,Mingliang Zhou,Qiming Li,Hui Li,Wei Duan,Xue Li,Yonghong Feng,Jianping Xie
Tuberculosis (TB), caused by Mycobacterium tuberculosis , remains a formidable threat to global public health . The successful intracellular persistence of M . tuberculosis significantly contributes to the intractability of tuberculosis. Proline-glutamic acid (PE) and proline-proline-glutamic acid (PPE) are mycobacterial exclusive protein families that widely reported to be involved in the bacterial virulence , physiology and interaction with host. Rv2770c (PPE44), a predicted virulence factor , was up-regulated upon the infected guinea pig lungs. To investigate the role of Rv2770c, we heterologously expressed the PPE44 in the nonpathogenic fast-growing M . smegmatis strain. Subcellular location analysis demonstrated that Rv2770c is a cell wall associated protein, suggestive of a potential candidate involved in host-pathogen interaction. The Rv2770c can enhance M . smegmatis survival within macrophages and under stresses such as H 2 O 2 , SDS, diamide exposure, and low pH condition. M . smegmatis expressing Rv2770c is more virulent as testified by the increased death of macrophages and the increased expression of interlukin-6 (IL-6) and interlukin-12p40 (IL-12p40). Moreover, Rv2770c altered the secretion of IL-6 and IL-12p40 of macrophages via NF-κB, ERK1/2 and p38 MAPK axis. Taken together, this study implicated that Rv2770c was a virulent factor actively engaged in the interaction with host macrophage.
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Bioengineered
·
2022
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IF 6.832
Miao Zhang,Chengkun Yin,Yan Chen,Juan Wang,Jing Jiang
Triggering receptor expressed on myeloid cells 1 (TREM1) participates in the development of endometritis. This study aims at identifying the effects and interaction of TREM1 and upstream stimulatory factor 2 (USF2) in endometritis by using a model of lipopolysaccharide (LPS)-induced human endometrial epithelial cells (HEnEpCs). ELISA was performed to determine the levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF-α) after LPS stimulation. TREM1 and USF2 expression was examined with RT-qPCR and Western blot. The JASPAR database was employed to predict the binding site between USF2 and TREM1, which was confirmed by luciferase reporter and chromatin immunoprecipitation assays. After TREM1 overexpression, IL-6, IL-1β, and TNF-α expression was detected by ELISA. Next, the binding of TREM1 to toll-like receptor (TLR) 2/4 was examined with co-immunoprecipitation. Then, proteins in TLR2/4-nuclear factor-kappaB (NF-κB) signaling in HEnEpCs under LPS condition were assessed by Western blot or immunofluorescence before and after TREM1 knockdown. Finally, TLR2 or TLR4 was silenced to explore whether intervene TLR2/4-NF-κB signaling pathway could rescue TREM1-overexpression-induced inflammation in LPS-induced HEnEpCs. Results revealed that upregulated TREM1 was observed in LPS-challenged HEnEpCs. Next, USF2 was found to have transcriptionally active TREM1 expression. Additionally, USF2 knockdown decreased the levels of IL-6, IL-1β, and TNF-α, whereas this effect was rescued after TREM1 overexpression. Besides, TREM1 could bind to TLR2/4 to regulate NF-κB signaling. Moreover, the intervention of TLR2/4-NF-κB signaling pathway rescued TREM1-overexpression-induced inflammation in LPS-stimulated HEnEpCs. Collectively, USF2 promotes endometritis by upregulating TREM1, thereby activating TLR2/4-NF-κB pathway.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2022
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IF 5.895
Fanghua Guo,Li Peng,Hua Xiong,Jiaqi Wang,Rong Tsao,Xin Peng,Li Jiang,Yong Sun
Polyphenol-rich Laird lentil hulls are a byproduct of lentil processing. In the present study, free and bound polyphenols in lentil hulls were analyzed with UHPLC-LTQ-OrbiTrap-MS2, and the anti-inflammatory mechanism of their digestive products was explored based on the NF-κB and Keap1-Nrf2 signaling pathways in the HT-29 cell model. In summary, a total of 27 polyphenols and 5 nonphenolic constituents were identified in free and bound fractions, and among them, catechin glucoside, kaempferol tetraglucoside, procyanidin dimer, and dihydroxybenzoic acid-O-dipentoside were the main polyphenols in the digestive products. These digestive products could reduce inflammatory mediators and exert anti-inflammatory activity by inhibiting NF-κB and activating Keap1-Nrf2 signaling pathways, and there was crosstalk between them, which was a mutual inhibition effect. The results show that polyphenols in lentil hulls are a good source of anti-inflammatory ingredients and have a promising development potential.
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JOURNAL OF MEDICINAL CHEMISTRY
·
2023
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IF 7.3
Jing Liao,Jun Yang,Xiaobo Li,Chenghong Hu,Weiwei Zhu,Ying Zhou,Yu Zou,Mi Guo,Zhichao Chen,Xiang Li,Jintian Dai,Yuye Xu,Zhiwei Zheng,Pan Chen,Won-Jea Cho,Guang Liang,Qidong Tang
Acute lung injury (ALI) and sepsis are both serious and complex conditions associated with high mortality, yet there are no effective treatments. Herein, we designed and synthesized a series of diphenyl 6-oxo-1,6-dihydropyridazine-3-carboxylate/carboxamide analogues exhibiting anti-inflammatory activity. The optimal compound J27 decreased the release of TNF-α and IL-6 in mouse and human cells J774A.1 and THP-1 (IL-6 IC50 = 0.22 μM) through the NF-κB/MAPK pathway. J27 demonstrated remarkable protection against ALI and sepsis in vivo and exhibited good safety in subacute toxicity experiments. Pharmacokinetic study indicated that J27 had good bioavailability (30.74%). To our surprise, J27 could target JNK2 with a totally new molecular skeleton compared with the only few JNK2 inhibitors reported. Moreover, there is no report that JNK2 inhibitors could apply for ALI and sepsis. Therefore, this work provides a new lead structure for the study of JNK2 inhibitors and a new target of JNK2 to treat ALI and sepsis.
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