Small
·
2023
·
IF 13.3
Yixuan Huang,Shuai He,Sheng Yu,Hannah M. Johnson,Yau Kei Chan,Zheng Jiao,Shouteng Wang,Zixiang Wu,Yi Deng
Although antibiotic is still the main choice for antibacteria both in hospital and community, phototherapy has become a possibly one of the alternative approaches in the treatment of microbe-associated infections nowadays because of its considerable potential in effective eradication of pathogenic bacteria. However, overwhelming reactive oxygen species (ROS) generated from phototherapy inevitably provoke an inflammatory response, complicating the healing process. To address this outstanding issue, a MXene-decorated nanofibrious is devised that not only yield localized heat but also elevate ROS levels under near-infrared laser exposure ascribed to the synergistic photothermal/photodynamic effect, for potent bacterial inactivation. After being further loaded with aspirin, the nanofibrous membranes exhibit benign cytocompatibility, boosting cell growth and suppressing the (nuclear factor kappa-B ( NF-κB) signaling pathways through RNA sequencing analysis, indicating an excellent anti-inflammatory effect. Interestingly, in vivo investigations also corroborate that the nanofibrous membranes accelerate infectious cutaneous regeneration by efficiently killing pathogenic bacteria, promoting collagen deposition, boosting angiogenesis, and dampening inflammatory reaction via steering NF-κB pathway. As envisaged, this work furnishes a decorated nanofibrous membrane with programmed antibacterial and anti-inflammatory effects for remedy of refractory bacteria-invaded wound regeneration.
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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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.
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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.
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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.
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PULMONARY PHARMACOLOGY & THERAPEUTICS
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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.
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Food & Function
·
2020
·Vol. 11
·期 12
·10852-10863
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IF 4.171
Mingbao Gu,Jie Jin,Chenghao Ren,Ximiao Chen,Weiyang Gao,Xiangyang Wang,Yaosen Wu,Naifeng Tian,Zongyou Pan,Aimin Wu,Yifei Zhou,Xiaolei Zhang
As an ordinary joint vestigial disease, osteoarthritis (OA) contributes to a considerable proportion of disability cases worldwide. Inflammation, as the main pathological factor, mediates the occurrence and development of OA. Akebia Saponin D (ASD), also known as Asperosaponin VI, is one of the active components extracted from Dipsaci Radix and is rich in Dipsacus loose tea. It has shown sound therapeutic effects on various diseases; nevertheless, its role in OA therapy is not completely understood. This study demonstrated the anti-inflammatory activity of ASD in OA through a series of in vivo and in vitro experiments. In vitro experiments revealed that ASD might prohibit the production of inflammatory mediators in IL-1β treated chondrocytes such as COX-2, iNOS, NO, PGE2, IL-6, and TNF-α. Meanwhile, it may also inhibit the production of ADAMTS-5 and MMP13 and promote the production of Aggrecan and Collagen II. The mechanism study demonstrated that ASD exerted an anti-inflammatory effect by activating the NRF2 target, upregulating the expression of HO-1, and preventing P65 from binding to DNA. In vivo experiments demonstrated that ASD might improve the progression of OA in a DMM mouse model. These research results provide evidence for the potential application of ASD in OA therapy.
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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.
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Marine Drugs
·
2020
·Vol. 18
·期 6
·328
·
IF 4.073
Jing Ye,Donghui Chen,Zhicheng Ye,Yayan Huang,Na Zhang,Edmund M. K. Lui,Changhu Xue,Meitian Xiao
Fucoidan has been reported to have a variety of biological activities. However, different algae species, extraction methods, harvesting seasons, and growth regions lead to the structural variation of fucoidan, which would affect the bioactivities of fucoidan. To date, the anti-inflammatory properties and the underlying mechanism of fucoidan from brown algaSaccharina japonica(S. japonica) remain limited. The aims of the present study were to investigate the structure, the anti-inflammatory properties, and the potential molecular mechanisms of fucoidan isolated fromS. japonica(SF6) against lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. SF6 was characterized using high performance liquid gel permeation chromatography (HPGPC), Fourier transform infrared spectroscopy (FTIR), and nuclear magnetic resonance spectroscopy (NMR), and observed to be rich in fucose, galactose, and sulfate. Additionally, results showed that SF6 remarkably inhibited LPS-induced production of various inflammatory mediators and pro-inflammation cytokines, including nitric oxide (NO), NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), interleukin-β (IL-β), and interleukin-6 (IL-6). A mechanism study showed that SF6 could effectively inhibit inflammatory responses through blocking LPS-induced inflammation pathways, including nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and Janus kinase (JAK)-2 and signal transducer and activator of transcription (STAT)-1/3 pathways. These results suggested that SF6 has the potential to be developed as an anti-inflammatory agent applied in functional food.Keywords:fucoidan;Saccharina japonica;anti-inflammation;mechanism
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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.
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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
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NEUROSCIENCE
·
2019
·
IF 3.244
Lanqiu Zhang,Jinlu Zhang,Xiaolin Jiang,Lei Yang,Qi Zhang,Botao Wang,Lihua Cui,Ximo Wang
Neuroinflammation has been implicated in the mechanism underlying the progression of neurodegeneration and infectious neuropathology. Growing evidence suggest that hydroxytyrosol (3,4-dihydroxyphenil-ethanol, HT), one of the main polyphenols presented in extra virgin olive oil (EVOO), has shown potential anti-inflammatory and neuroprotective effects. However, the potential anti-neuroinflammation activity and underlying mechanism of HT remain poorly understood. The present study aimed to investigate the effects of HT on lipopolysaccharide (LPS)-induced inflammation in both in vitro and in vivo models and the associated molecular mechanism. Our results revealed that HT significantly reduced the production of pro-inflammatory mediators in BV2 microglia and primary microglia cells. Phenotypic analysis showed that HT significantly reduced M1 marker CD86 expression and increased M2 marker CD206 expression. In addition, HT significantly decreased the levels of phospho-NF-κB p65 and phospho-extracellular signal-regulated kinase (ERK) in a dose-dependent manner. Moreover, HT suppressed the LPS-induced Toll like receptor 4 (TLR4) in BV2 microglia. In vivo administration of HT following LPS injection significantly reduced some proinflammatory mediator levels and microglia/astrocyte activation in the brain. Together, these results suggest that HT suppressed the LPS-induced neuroinflammatory responses via modulation of microglia M1/M2 polarization and downregulation of TLR-4 mediated NF-κB activation and ERK signaling pathway.
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FOOD AND CHEMICAL TOXICOLOGY
·
2018
·
IF 3.977
Jian Fang,Qiuyan Chen,Baozhu He,Jiaxuan Cai,Yawen Yao,Yi Cai,Suowen Xu,Kannan R.R. Rengasamy,Shanmugaraj Gowrishankar,Shunmugiah Karutha Pandian,Tiansheng Cao
Tanshinone IIA is one of the most predominant bioactive constituents of Danshen , a traditional Chinese medicinal plant with multiple cardiovascular protective actions. Although Tanshinone IIA has been well documented for its endothelial protective efficacy, studies unveiling the mechanism and/or molecular targets for its pharmacological activity are still inadequate. In recent studies, it has been envisaged that the expression of pentraxin 3 (PTX3) was associated with atherosclerotic cardiovascular diseases (ACVD). Therefore, the current study was designed to evaluate the possible role of Tanshinone IIA in influencing the expression of PTX3 in endothelial cells and thereby prevents endothelial dysfunction . Molecular analyses through real-time PCR, western blot , and ELISA revealed that Tanshinone IIA down-regulates PTX3 gene expression as well as protein secretion in human endothelial cells in the presence or absence of TNF-α. Besides, Tanshinone IIA inhibits the adhesion of THP1 cells (a monocytic cell line) to activated-endothelial cells stimulated with TNF-α. Furthermore, mechanistic studies uncovered the role of p38 MAPK/NF-κB pathway in Tanshinone II-A mediated pharmacological effects. Thus, the present study exemplifies the manifestation of Tanshinone IIA as a plausible alternative natural remedy for ACVD by targeting PTX3.
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