SCIENCE OF THE TOTAL ENVIRONMENT
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2023
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IF 9.8
Lu Jiang,Fan Yang,Huan Liao,Weiwei Chen,Xueyan Dai,Chengcheng Peng,Zhiyuan Li,Huating Wang,Tao Zhang,Huabin Cao
In this study, 24 healthy male sheep were divided into four groups: the control group, Mo group (45 mg Mo·kg-1·BW), Cd group (1 mg Cd·kg-1·BW), and Mo + Cd group (45 mg Mo·kg-1·BW + 1 mg Cd·kg-1·BW). The experiment was last for 50 d. The results showed that Mo and Cd co-exposure induced histopathological changes and ultrastructural damage, decreased the mRNA and protein expression levels of BTB (blood-testis barrier)-related factors (CX-43, ZO-1, OCLN) ( P < 0.05) and the T-SOD and CAT activity (P < 0.05), increased the MDA content (P < 0.05) and the proinflammatory factors levels (P < 0.05) in sheep testes. Moreover, the results showed that a sharp decline in BTB-related factors and antioxidase activity, and a significant increase in reactive oxygen species (ROS) levels ( P < 0.05) and the expression levels of NLRP3 inflammasome-related factors (P < 0.05) in primary Sertoli cells (SCs) under Mo and Cd co-exposure. However, treatment with a ROS scavenger or NLRP3 inflammasome inhibitors could relieve BTB damage and oxidative injury, reduce the production of ROS ( P < 0.05) and decrease the level of inflammatory factors (P < 0.05). Overall, these results indicated that Mo and Cd co-exposure reduced BTB-related protein levels and promoted ROS production and inflammatory reactions by activating the ROS/NLRP3 inflammasome pathway in sheep testes, which eventually induced reproductive toxicity.
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PHYTOMEDICINE
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2023
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IF 7.9
MinChao Feng,BaiJun Qin,Fang Luo,Hui Li,KunRong Liu,Kai Li,DongYang Wu,XiPing Tang,Guozhong Chen
Background Safer and more effective drugs are needed for the treatment of acute pancreatitis (AP). Qingjie Huagong decoction (QJHGD) has been applied to treat AP for many years and has shown good clinical effects. However, the potential mechanism has not yet been determined. Purpose To investigate the role and underlying mechanism of the effects of QJHGD on AP both in vitro and in vivo . Methods QJHGD was characterized by UHPLC-Q-Orbitrap-MS. The protective effect of QJHDG and the underlying mechanism were investigated in MPC-83 cells in vitro . A caerulein-induced AP model was established to evaluate the protective effect of QJHGD in mice. CCK-8 assays were used to detect cell viability. The contents of inflammatory mediators were determined by ELISA. Expression levels of circRNA, miRNA and mRNA were determined by qRT-PCR. Protein expression was determined using Western blot . Pancreatic tissues were assessed by hematoxylin and eosin staining as well as immunohistochemical and immunofluorescence analyses. Pull-down and luciferase activity assays were performed to determine the regulatory relationships of circHipk3, miR-193a-5p and NLRP3. Results Our results confirmed that mmu-miR-193a-5p was sponged by mmu-circHipk3, and NLRP3 was a target of miR-193a-5p. In vitro experiments showed that QJHGD enhanced MPC-83 cell viability by regulating circHipk3 sponging mir-193a-5 targeting NLRP3 and inhibiting pyroptosis-related factors. Finally, we showed that QJHGD ameliorated pancreatic tissue injury in AP mice via this pathway. Conclusion This study demonstrate that QJHDG exerted its anti-AP effects via the circHipk3/miR-193a-5p/NLRP3 pathway, revealing a novel mechanism for the therapeutic effect of QJHDG on AP.
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NATURAL PRODUCT RESEARCH
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2023
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IF 2.2
De-Wen Bi,Jian- Feng,Wen-Hui Pang,Peng-Yun Yang,Yao-Jun Xu,Muhammad Aurang Zeb,Meng-Ru Wang,Xing-Jie Zhang,Xiao-Li Li,Rui-Han Zhang,Wei-Guang Wang,Wei-Lie Xiao
Three new lanostane triterpenoids (1-3) along with two new amides fatty compounds (4-5) were isolated from the ethyl acetate extract of a culture of the endophytic fungus Alternaria sp. gx-2. Their structures were identified by 1D and 2D NMR spectral data and HRESIMS. Compounds 1-12 were evaluated for their anti-inflammatory and tyrosinase inhibition activities. The isolated compounds did not show inhibitory activities at a concentration of 100 μM against tyrosinase, while under the concentration of 10 μM, the release of lactate dehydrogenase (LDH) inhibition rate of compound 1 was 54.45%, indicating that compound 1 had moderate anti-inflammatory activity on the activation of NLRP3 inflammasome.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2023
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IF 8.2
Qun Wang,Zhaomei Wang,Jun Song,Kangjie Xu,Wenni Tian,Xu Cai,Jiamei Mo,Yong Cao,Jie Xiao
A nanolipidcarrier (NLC) loaded homogalacturonan enriched pectin (citrus modified pectin, MCP4) hydrogel was designed as a novel colon inflammation site-specific oral delivery system for 6-gingerol (6G) (6G-NLC/MCP4 hydrogel) administration, and its colitis alleviation effect were investigated. 6G-NLC/MCP4 exhibited typical “cage-like” ultrastructure with 6G-NLC embedded in the hydrogel matrix as observed by cryoscanning electron microscope. And due to the homogalacturonan (HG) domain in MCP4 specifically combined with Galectin-3, which is overexpressed in the inflammatory region, the 6G-NLC/MCP4 hydrogel targeted to severe inflammatory region. Meanwhile, the prolonged-release characteristics of 6G-NLC provided sustained release of 6G in severe inflammatory regions. The matrix of hydrogel MCP4 and 6G achieved synergistic alleviation effects for colitis through NF-κB/NLRP3 axis. Specifically, 6G mainly regulated the NF-κB inflammatory pathway and inhibited the activity of NLRP3 protein, while MCP4 regulated the expression of Galectin-3 and peripheral clock gene Rev-Erbα/β to prevent the activation of inflammasome NLRP3.
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AMERICAN JOURNAL OF CHINESE MEDICINE
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2023
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IF 5.7
Xingguan Yang,Jiahui Han,Zhirong Huan,Ce Xu,Qiubo Wang,Xin Ge
Hemorrhagic shock (HS) is defined as a reduction in tissue oxygenation and organ dysfunction due to severe blood loss. Lung injury is a frequent complication of HS. Baicalin, isolated from Radix Scutellariae , has been reported to profile the antitumor, anti-oxidative, anti-inflammatory, and antibacterial roles in various pathological processes. Nevertheless, the effects of baicalin on HS-induced lung injury are unclear. This study aims to examine the therapeutic effects of baicalin on lung injury. We first established the lung injury rat models by withdrawing blood in the femoral artery followed by resuscitation. A pathological analysis showed that HS-administrated rats presented severe capillary leakage and pulmonary edema, while baicalin therapy alleviated the symptoms. Baicalin therapy reduced the number of macrophages and neutrophils in bronchoalveolar lavage fluid and decreased the expression and activity of myeloperoxidase (neutrophile infiltration marker) in the lung tissues of HS rats, indicating that baicalin alleviated HS-induced infiltration of inflammatory cells. The secretion of inflammatory cytokines, including interleukin (IL)-1 β , IL-6, IL-18, and tumor necrosis factor α (TNF- α ), as well as the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3 (NLRP3) inflammasome, were inhibited by baicalin administration. Furthermore, we found that the NF- κ B pathway, a canonical pro-inflammatory pathway, was also blocked after treatment with baicalin in HS-evoked rats, as indicated by the decreased expression of p65 and p65 phosphorylation in the lung tissues. In summary, we infer that baicalin may exert a protective role in HS-induced lung injury by suppressing the activation of NLRP3 inflammasome via the NF- κ B pathway.
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NEUROTOXICITY RESEARCH
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2022
·Vol. 40
·期 1
·78-88
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IF 3.978
Ji Na,Wu Lirong,Shi Hui,Li Qianlu,Yu Anyong,Yang Zhao
Intracerebral hemorrhage (ICH) is a fatal cerebrovascular disease. Neuroinflammation plays an important pathological role in brain injury after ICH. NLRP3 contributes to the pathogenesis of ICH, but the underlying mechanisms regulating of NLRP3 remain elusive. V-set and immunoglobulin domain containing 4 (VSIG4), specifically expressed in resting tissue-resident macrophages, can deliver anti-inflammatory signals into various inflammatory diseases. However, the interaction between VSIG4 and NLRP3, as well as the underlying mechanisms after ICH have not been reported. C57BL/6 mice were subjected to the autologous blood injection ICH model. VSIG4 and NLRP3 levels of macrophages were detected following ICH. Ad-VSIG4 or controls were administered via intracerebroventricular (i.c.v) injection before ICH induction. STAT3 inhibitor (S31-201), JAK2 inhibitor (TG101348), or Ad-A20 RNAi was administered to investigate the role of JAK2-STAT3-A20 pathway in VSIG4-mediated neuroinflammation after ICH. Pro-inflammatory cytokine production, BBB disruption, brain water content, and neurological test were examined in ICH mice. VSIG4 levels were significantly decreased, and NLRP3 levels were significantly increased in the perihematomal brain tissues after ICH. Ad-VSIG4 attenuated NLRP3 levels and inhibited inflammation, as well as improved neurological function and reduced BBB disruption and brain water content. Furthermore, Ad-VSIG4 increased the protein levels of phosphorylated JAK2 and STAT3, and A20 levels at 24 h after ICH. STAT3 inhibitor, JAK2 inhibitor, and A20 RNAi abolished the beneficial effects of Ad-VSIG4 after ICH. In summary, these data suggested that VSIG4 attenuated NLRP3 and ameliorated neuroinflammation via JAK2-STAT3-A20 pathway after intracerebral hemorrhage in mice. VSIG4 might be an ideal therapeutic target for ICH patients.
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INTERNATIONAL IMMUNOPHARMACOLOGY
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2021
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IF 4.932
Jin Zhang,Changsong Wang,Hongliang Wang,Xueting Li,Jingjing Xu,Kaijiang Yu
Sepsis is a systemic inflammatory response syndrome resulted from severe infection. Excessive inflammation response plays an important role in sepsis-induced acute lung injury (ALI). Loganin is an iridoid glycoside isolated from Corni fructus and exerts an anti-inflammatory effect in multiple inflammatory diseases; however, the role of loganin in sepsis-induced ALI remains unknown. In the current study, the cecal ligation and puncture (CLP)-induced murine sepsis model was constructed to investigate the anti-inflammatory property of loganin in sepsis-induced ALI. Lipopolysaccharide (LPS)-treated Raw 264.7 cells and primary murine peritoneal macrophages were established to further explore underlying mechanism of loganin. Results showed that intragastrical administration of loganin significantly increased murine survival, reduced the alveolar structure damage and inflammatory cell infiltration. Loganin suppressed the release of the M1 macrophage-associated pro-inflammatory cytokines and induced the activation of M2-type anti-inflammatory cytokines. Besides, loganin dramatically inhibited NLRP3 inflammasome-mediated caspase-1 activation and subsequent IL-1β secretion. Further in vitro studies confirmed that loganin efficiently inhibited M1 macrophage polarization and NLRP3 inflammasome activation by blocking the extra-cellular signal-regulated kinase (ERK) and nuclear factor-kappa B (NF-κB) pathways. Taken together, the anti-inflammatory effect of loganin in sepsis-induced ALI was associated with the ERK and NF-κB pathway-mediated macrophage polarization and NLRP3 inflammasome activation. Our study offers a favorable mechanistic basis to support the therapeutic potential of loganin in anti-inflammatory diseases, such as sepsis-induced ALI.
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METABOLISM-CLINICAL AND EXPERIMENTAL
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2021
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IF 8.697
Suling Huang,Yanwei Wu,Zhuohui Zhao,Bing Wu,Kai Sun,Haoyu Wang,Li Qin,Fang Bai,Ying Leng,Wei Tang
Objective Obeticholic acid (OCA) has been proved to play potential therapeutic effect on nonalcoholic steatohepatitis (NASH). Up to now, the study of OCA on NLRP3 inflammasome activation in macrophage is still blank and merits great attention. Here, we aimed to better characterize the role and mechanism of OCA on NASH treatment focusing on NLRP3 inflammasome activation in macrophages. Methods The effects of OCA on inflammasome activation were investigated in BMDM , Kupffer cell , BMDC and LX2 cell. Preconditioned media from BMDM culture was used to treat primary hepatocytes to explore the effects of macrophage NLRP3 inflammasome activation on the function of hepatocytes. In vivo, high fat diet plus CCl 4 (DIO + CCl 4 ) induced murine NASH model and choline-deficient and amino acid-defined (CDA) diet-induced NASH mice were used to verify the inhibitory effect of OCA on inflammasome activation in liver macrophages and recapitulate its protective role on NASH progressing. To clear up the effect of OCA on macrophage is FXR dependent or not, FXR siRNA was introduced into BMDMs. Results OCA blockaded NLRP3 inflammasome in BMDMs by impacting on the activation stage and disrupting ASC oligomerization . Preconditioned supernatant from LPS + ATP treated BMDMs increased mRNA expression of lipogenic enzymes and lipid content, whereas preconditioned supernatant from OCA treated BMDM blocked these effects in both normal and the FXR knockdown hepatocytes. In DIO + CCl 4 mice, the population of inflammatory myeloid lineage cells in livers was decreased upon OCA treatment. Accordingly, the level of IL-1β and IL-18 in liver, the hepatic expression of ASC, pro-caspase-1 and active caspase-1, the expression of caspase 1 p20 in liver macrophages were also reduced. Similar results were obtained in CDA diet-fed mice. Furthermore, OCA maintained the inhibition on NLRP3 inflammasome activation in FXR knockdown BMDMs, suggesting FXR could be dispensable in this effect. Conclusions This finding brings up a new mechanism of OCA on NASH treatment, suggested by direct inhibition on NLRP3 inflammasome activation in macrophage, further suppression on inflammasome activation-elicited hepatic lipid accumulation , and contributing to the amelioration of NASH.
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Oxidative Medicine and Cellular Longevity
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2021
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IF 6.543
Jin-jin Zhu,Bin-yuan Yu,Xiao-kai Huang,Min-zhi He,Bin-wen Chen,Ting-ting Chen,Huang-yi Fang,Shang-qin Chen,Xiao-qin Fu,Pei-jun Li,Zhen-lang Lin,Jiang-hu Zhu
Hypoxic-ischemic encephalopathy (HIE) is recognized as the main cause of neonatal death, and efficient treatment strategies remain limited. Given the prevalence of HIE and the associated fatality, further studies on its pathogenesis are warranted. Oxidative stress and neuroinflammatory injury are two important factors leading to brain tissue injury and nerve cell loss in HIE. Neferine, an alkaloid extracted from lotus seed embryo, exerts considerable effects against several diseases such as cancers and myocardial injury. In this study, we demonstrated the neuroprotective effect of neferine on HIE and hypothesized that it involves the inhibition of neuronal pyroptosis, thereby ameliorating neurological inflammation and oxidative stress. We demonstrated that the mRNA levels of proteins associated with pyroptosis including caspase-1, the caspase adaptor ASC, gasdermin D, interleukin- (IL-) 18, IL-1β, and some inflammatory factors were significantly increased in neonatal HIBD model rats compared to those in the control group. The increase in these factors was significantly suppressed by treatment with neferine. We stimulated PC12 cells with CoCl2 to induce neuronal HIBD in vitro and investigated the relationship between neferine and pyroptosis by altering the expression of the NLRP3 inflammasome. The overexpression of NLRP3 partially reversed the neuroprotective effect of neferine on HIBD, whereas NLRP3 knockdown further inhibited caspase-1 activation and IL-1β and IL18 expression. In addition, simultaneous alteration of NLRP3 expression induced changes in intracellular oxidative stress levels after HIBD. These findings indicate that neferine ameliorates neuroinflammation and oxidative stress injury by inhibiting pyroptosis after HIBD. Our study provides valuable information for future studies on neferine with respect to neuroinflammation and pyroptosis.
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Microbiome
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2019
·Vol. 7
·期 1
·1-16
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IF 10.465
Zhang Yuan,Huang Rongrong,Cheng Mengjing,Wang Lirui,Chao Jie,Li Junxu,Zheng Peng,Xie Peng,Zhang Zhijun,Yao Honghong
Background Inflammasomes have been found to interact with the gut microbiota, and this effect is associated with depression, but the mechanisms underlying this interaction have not been elucidated in detail.Results The locomotor activity of NLRP3 KO mice was significantly greater than that of their WT littermates, while cohousing and transplantation of the NLRP3 KO gut microbiota avoid the effects of NLRP3 KO on the general locomotor activity at baseline. Meanwhile, transplantation of the NLRP3 KO microbiota alleviated the CUS-induced depressive-like behaviors. The compositions of the gut microbiota in NLRP3 KO mice and WT mice were significantly different in terms of the relative abundance of Firmicutes, Proteobacteria, and Bacteroidetes. Fecal microbiota transplantation (FMT) from NLRP3 KO mice significantly ameliorated the depressive-like behavior induced by chronic unpredictable stress (CUS) in recipient mice. Given the correlation between circular RNA HIPK2 (circHIPK2) and depression and the observation that the level of circHIPK2 expression was significantly increased in CUS-treated mice compared with that in the control group, further experiments were performed. FMT significantly ameliorated astrocyte dysfunction in recipient mice treated with CUS via inhibition of circHIPK2 expression.Conclusion sOur study illustrates the involvement of the gut microbiota-circHIPK2-astrocyte axis in depression, providing translational evidence that transplantation of the gut microbiota from NLRP3 KO mice may serve as a novel therapeutic strategy for depression.
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Autophagy
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2019
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IF 11.059
Xiaojuan Han,Sifan Sun,Yiming Sun,Qiqi Song,Jialei Zhu,Nanshan Song,Miaomiao Chen,Ting Sun,Meiling Xia,Jianhua Ding,Ming Lu,Honghong Yao,Gang Hu
Aging-related, nonresolving inflammation in both the central nervous system (CNS) and periphery predisposes individuals to the development of neurodegenerative disorders (NDDs). Inflammasomes are thought to be especially relevant to immune homeostasis, and their dysregulation contributes to inflammation and NDDs. However, few agents have been clinically shown to reduce NDD incidence by targeting inflammasomes. Our study indicated that NLRP3 (NLR family, pyrin domain containing 3) inflammasome is involved in Parkinson disease (PD) progression in patients and various murine models. In addition, the small molecule kaempferol (Ka) protected mice against LPS- and SNCA-induced neurodegeneration by inhibiting NLRP3 inflammasome activation as evidenced by the fact that Ka reduced cleaved CASP1 expression and disrupted NLRP3-PYCARD-CASP1 complex assembly with concomitant decreased IL1B secretion. Mechanically, Ka promoted macroautophagy/autophagy in microglia, leading to reduced NLRP3 protein expression, which in turn deactivated the NLRP3 inflammasome. Intriguingly, ubiquitination was involved in Ka-induced autophagic NLRP3 degradation. These findings were further confirmed in vivo as knockdown of Atg5 expression or autophagy inhibitor treatment significantly inhibited the Ka-mediated NLRP3 inflammasome inhibition and neurodegeneration amelioration. Thus, we demonstrated that Ka promotes neuroinflammatory inhibition via the cooperation of ubiquitination and autophagy, suggesting that Ka is a promising therapeutic strategy for the treatment of NDDs.Abbreviations: 3-MA: 3-methyladenine; AAV: adeno-associated virus; ACTB: actin, beta; AIF1/IBA1: allograft inflammatory factor 1; ATG5: autophagy related 5; ATG7: autophagy related 7; BafA1: bafilomycin A1; BECN1: beclin 1, autophagy related; CASP1: caspase 1; CNS: central nervous system; CQ: chloroquine; DA neurons: dopaminergic neurons; DAMPS: damage-associated molecular patterns; DAPI: 4’,6-diamidino-2-phenylindole; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GFP: green fluorescent protein; GFAP: glial fibrillary acidic protein; IP: immunoprecipitation; i.p.: intraperitoneally; Ka: kaempferol; KD: knockdown; KO: knockout; LPS: lipopolysaccharide; IL1B: interleukin 1 beta; IL6: interleukin 6; Ly: lysate; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MPTP: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; NC: negative control; NDD: neurodegenerative diseases; NLRP3: NLR family, pyrin domain containing 3; OE: overexpression; PD: Parkinson disease; poly-Ub: poly-ubiquitin; PTM: post-translational modification; PYCARD/ASC: PYD and CARD domain containing; Rapa: rapamycin; RFP: red fluorescent protein; SN: supernatant; SNCA: synuclein alpha; SNpc: substantia nigra pars compacta; SQSTM1: sequestosome 1; TH: tyrosine hydroxylase; TNF/TNF-alpha: tumor necrosis factor; Ub: ubiquitin; WT: wild type
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JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Su Li,Caolin Zhong,Wei Jiang,Baojun Zheng,Ruoxin Xiang,Beixuan Yang,Chaozhan Lin,Chenchen Zhu,Meiqi Wang
Ethnopharmacological relevance Huzhang Erjin Decoction (HED) is a Traditional Chinese Medicine (TCM) Formula that possesses the efficiency of clearing heat, eliminating dampness, purging the liver and gallbladder. It has been clinically used in the treatment of inflammation related to hepatobiliary disease, including cholestasis, cholecystitis and jaundice. However, the mechanism of HED for its therapeutic effects has not been explored. Aim of the study This study aimed to investigate the potential mechanism of HED in ameliorating cholestatic hepatitis based on an integrative approach with metabolomics and network pharmacology. Materials and methods In this study, the pharmacodynamic effect of HED was evaluated based on alpha-naphthylisothiocyanate (ANIT)-induced cholestatic hepatitis mice. Furthermore, network pharmacology analysis was conducted to explore the potential mechanism of HED. Meanwhile, serum metabolomics analysis was performed to investigate the key metabolic pathways and biological processes regulated by HED. Furthermore, related targets and pathways were focused, according to a comprehensive analysis combined with metabolomics and network pharmacology. Molecular docking simulations were performed to evaluate the interactions between components of HED and the targets against cholestatic hepatitis. Finally, the regulatory effects of HED on the expression levels of key proteins in the peroxisome proliferator-activated receptor gamma (PPARγ) and NOD-like receptor thermal protein domain associated protein 3 (NLRP3) pathways were investigated both in vitro and in vivo . Results Our research findings demonstrate that HED significantly enhances liver function and alleviates liver injury in cholestatic hepatitis mice, including bile acid accumulation, hepatic necrosis and inflammatory infiltration. Furthermore, according to the combined enrichment of network pharmacology analysis and metabolomics study, HED primarily modulates cholestatic hepatitis via the regulation of lipid metabolism and bile acid metabolism to intervene in cholestatic hepatitis. Additionally, molecular docking studies revealed a high affinity and activity between the hub gene PPARG (PPARγ) and emodin in HED. Furthermore, the in vivo and in vitro results demonstrated that HED significantly promoted the expression of PPARγ and decreased the expression levels of NLRP3 and its associated proteins. In vitro , suppression of PPARγ attenuated the efficacy of HED. These findings suggested that HED modulated the PPARγ/NLRP3 signaling pathway, thereby improving cholestatic hepatitis and alleviating liver injury. Conclusion This study systematically assessed the efficacy of HED in the intervention of cholestatic hepatitis and explored the targets by integrating metabolomics and network pharmacology approaches, then elucidated its mechanism based on experiments both in vitro and in vivo . It was demonstrated that HED ameliorated cholestatic hepatitis in mice by regulating the PPARγ/NLRP3 pathway.
研究领域:
中药学
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药理学
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代谢组学
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生物信息学
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