ACTA BIOCHIMICA ET BIOPHYSICA SINICA
·
2021
·Vol. 53
·期 12
·1590-1601
·
IF 3.848
Yu Guili,Wang Jinxin,Zhang Wei,Yang Qiankun,Liu Gang,Wang Lei,Bello Babatunde Kazeem,Zhang Xiao,Zhang Tianmeng,Fan Hui,Zhao Panpan,Liang Wei,Dong Jingquan
Vibrio harveyi, an important zoonotic pathogen, can infect wounds and cause inflammatory response. Understanding the inflammatory response pathways could facilitate the exploration of molecular mechanisms for treating V. harveyi infection. NLR family pyrin domain-containing 3 (NLRP3) inflammasome is involved in the interaction between hosts and pathogenic microorganisms and could be sensed by various pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). Nonetheless, the function of NLRP3 inflammasome in V. harveyi infection remains unclear. In the present study, we established a V. harveyi infection model using murine peritoneal macrophages (PMs). Various techniques, including western blot analysis, enzyme-linked immunosorbent assay (ELISA), RT-qPCR, immunofluorescence, and inhibition assays, were used to explore the molecular mechanism of V. harveyi-induced inflammation. The results showed that many inflammatory cytokines participated in V. harveyi infection, with interleukin (IL)-1β being the most abundant. Pan-caspase inhibitor pretreatment significantly decreased the secretion of IL-1β in murine PMs. Moreover, the identification of V. harveyi involved a large number of NLR molecules, especially the NLRP3 receptor, and further studies revealed that NLPR3 inflammasome was activated by V. harveyi infection, as evidenced by puncta-like NLRP3 surrounding cell nuclear, ASC specks in the nucleus and cytoplasm, and ASC oligomerization. Inhibition of NLRP3 inflammasome impaired the release of mature IL-1β in V. harveyi-infected murine PMs. Furthermore, blocking the secretion of mature IL-1β could markedly decrease the release of other proinflammatory cytokines, including IL-6, IL-12, and tumor necrosis factor-α. Overall, these data indicated that NLRP3 inflammasome was activated in response to V. harveyi infection and enhanced inflammatory response by promoting IL-1β secretion in murine PMs.
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CARBOHYDRATE POLYMERS
·
2021
·
IF 9.381
Xianglin Pan,Haoyu Wang,Ziming Zheng,Xiao Huang,Linlin Yang,Junxi Liu,Kaiping Wang,Yu Zhang
Ulcerative colitis (UC) is an inflammatory bowel disease that affects the colon and rectum. Although galectin-3 (Gal-3) has been reported to play a proinflammatory role in UC, it is unknown whether pectic polysaccharide , a Gal-3 inhibitor in tumor metastasis, can alleviate UC by inhibiting Gal-3. The aim of this study was to investigate the anti-inflammatory effects and underlying mechanisms of SCLP, a pectic polysaccharide purified from Smilax china L. in our previous work, on dextran sulfate sodium-induced UC in BALB/c mice. The results showed that SCLP could significantly improve symptoms, alleviate histopathological damage and reduce the secretion of inflammatory mediators in mice with UC. Analysis of the anti-colitis mechanisms indicated that SCLP could inhibit the Gal-3/NLRP3 inflammasome/IL-1β pathway by suppressing the expression of Gal-3 and the interaction of Gal-3 and NLRP3 . Our results suggested that SCLP could be a promising candidate for prevention and treatment of UC.
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Frontiers in Pharmacology
·
2021
·
IF 5.811
Zhang Xueyan,Liu Yingbo,Deng Guangrui,Huang Bisheng,Kai Guoyin,chen Keli,Li Juan
Background: Activation of nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome plays a crucial role in gout. Selaginella moellendorffii has been confirmed effective for the treatment of gout in hospital preparations. Flavonoids, such as amentoflavone (AM), are the main active components of this medicine.Purpose: We aimed to investigate the flavonoid extract (TF) and AM's effects on NLRP3 inflammasome in vitro and their preventive effects on gout in vivo.Methods: LC-MS method was employed to investigate the chemical profile of TF. The cellular inflammation model was established by lipopolysaccharide (LPS) or monosodium urate (MSU) stimulation. The cell membrane integrality and morphological characteristics were determined by using Lactate dehydrogenase (LDH) assay kits, propidium iodide (PI) stain, and scanning electron microscopy (SEM). The inflammatory cytokines and NLRP3 inflammasome activation were determined using enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (RT-PCR), immunofluorescence staining, and western blotting. The acute gout mouse model was induced by MSU injection into footpads, and then the paw edema, inflammatory mediators, and histological examination (HE) were analyzed.Results: The main constituents in TF are AM and robustaflavone. In the cellular inflammation model, TF down-regulated the levels of nitric oxide (NO), TNF-α, and LDH, suppressed NLRP3 inflammasome-derived interleukin-1β (IL-1β) secretion, decreased caspase-1 activation, repressed mature IL-1β expression, inhibited ASC speck formation and NLRP3 protein expression. In an acute gout mouse model, oral administration of TF to mice effectively alleviated paw edema, reduced inflammatory features, and decreased the levels of IL-1β in mouse foot tissue. Similarly, the characteristic constituent AM was also able to down-regulated the levels of NO, TNF-α, and LDH, down-regulate the mRNA expression of IL-1β, TNF-α, caspase-1, and NLRP3. Besides, the foot thickness, lymphocyte infiltration, and IL-1β level were also prevented by AM.Conclusion: The results indicated that TF and its main constituent AM alleviate gout arthritis via NLRP3/ASC/Caspase-1 axis suppression.
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BIOMEDICINE & PHARMACOTHERAPY
·
2020
·
IF 4.545
Wen-Qiao Qiu,Rong Pan,Yong Tang,Xiao-Gang Zhou,Jian-Ming Wu,Lu Yu,Betty Yuen-Kwan Law,Wei Ai,Chong-Lin Yu,Da-Lian Qin,An-Guo Wu
Emerging evidence indicates that the enhancement of microglial autophagy inhibits the NLRP3 inflammasome mediated neuroinflammation in Alzheimer's disease (AD). Meanwhile, low density lipoprotein receptor-related protein 1 (LRP1) highly expressed in microglia is able to negatively regulate neuroinflammation and positively regulate autophagy. In addition, we have previously reported that an active lychee seed fraction enriching polyphenol (LSP) exhibits anti-neuroinflammation in Aβ-induced BV-2 cells. However, its molecular mechanism of action is still unclear. In this study, we aim to investigate whether LSP inhibits the NLRP3 inflammasome mediated neuroinflammation and clarify its molecular mechanism in Aβ-induced BV-2 cells and APP/PS1 mice. The results showed that LSP dose- and time-dependently activated autophagy by increasing the expression of Beclin 1 and LC3II in BV-2 cells, which was regulated by the upregulation of LRP1 and its mediated AMPK signaling pathway. In addition, both the Western blotting and fluorescence microscopic results demonstrated that LSP could significantly suppress the activation of NLRP3 inflammasome by inhibiting the expression of NLRP3, ASC, the cleavage of caspase-1, and the release of IL-1β in Aβ(1-42)-induced BV-2 cells. In addition, the siRNA LRP1 successfully abolished the effect of LSP on the activation of AMPK and its mediated autophagy, as well as the inhibition of NLRP3 inflammasome. Furthermore, LSP rescued PC-12 cells which were induced by the conditioned medium from Aβ(1-42)-treated BV-2 cells. Moreover, LSP improved the cognitive function and inhibited the NLRP3 inflammasome in APP/PS1 mice. Taken together, LSP inhibited the NLRP3 inflammasome-mediated neuroinflammation in the in vitro and in vivo models of AD, which was closely associated with the LRP1/AMPK-mediated autophagy. Thus, the findings from this study further provide evidences for LSP serving as a potential drug for the treatment of AD in the future.
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INTERNATIONAL IMMUNOPHARMACOLOGY
·
2020
·
IF 3.943
Yu Li,Rong Wang,Lian Xue,Yilin Yang,Feng Zhi
Background Ischaemic stroke is a lethal cerebrovascular disease that occurs worldwide. Astilbin is a natural flavonoid compound with various physiological activities. The purpose of this study was to investigate the neuroprotective effects of Astilbin after cerebral ischaemia reperfusion (I/R) injury. Methods The oxygen and glucose deprivation (OGD) model was used to simulate cerebral I/R injury in vitro . Cell viability was measured via CCK-8 and LDH release assays. Cell apoptosis was measured via Hoechst 33258 staining and flow cytometry assays. ROS was detected via flow cytometry assay. The protein expression levels were determined by western blotting. The middle cerebral artery occlusion (MCAO) model was used to simulate cerebral I/R injury in vivo . Cerebral ischaemic volume was measured by TTC staining. The Zea-Longa score, rota-rod test, and foot-fault test were used to evaluate behavioural changes and neurological deficits in rats. Results Astilbin significantly enhanced cell viability and decreased LDH release after OGD treatment in vitro . Astilbin effectively curbed cell apoptosis induced by OGD via inhibiting the activation of caspase-3, decreasing the ratio of Bax/Bcl-2 and decreasing FADD. Astilbin also inhibited OGD-induced inflammation by suppressing ROS-NLRP3 inflammasome axis activation. Further results revealed that Astilbin could suppress the MAPK pathway and activate the PI3K/AKT pathway. Finally, Astilbin significantly reduced the cerebral infarction volume and relieved neurological deficits in rats in vivo . Conclusion Astilbin could defend against cerebral I/R injury by inhibiting apoptosis and inflammation via suppressing the MAPK pathway and activating the AKT pathway.
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Hepatology International
·
2019
·Vol. 14
·期 1
·145-160
·
IF 5.49
Zhao Jing,Han Ming,Zhou Li,Liang Pu,Wang Yun,Feng Shenghu,Lu Hongping,Yuan Xiaoxue,Han Kai,Chen Xiaofan,Liu Shunai,Cheng Jun
Background This study aimed to investigate the roles and mechanisms of tenofovir alafenamide fumarate (TAF)/tenofovir disoproxil fumarate (TDF) in treating liver fibrosis. Methods The effects of TAF/TDF on carbon tetrachloride (CCl 4 )-induced liver fibrosis in C57BL/6 wild-type or nonstructural protein 5A transactivated protein 9 (NS5ATP9) knockout mice were studied. The differentiation, activation, and proliferation of LX-2 cells after TAF/TDF treatment were tested in vitro. The expression of NS5ATP9 and activities of transforming growth factor-β1 (TGFβ1)/Sekelsky mothers against decapentaplegic homolog 3 (Smad3) and NF-κB/NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome signaling pathways were detected in TAF/TDF-treated mice and LX-2 cells. The genes related to extracellular matrix accumulation were detected in vivo and in vitro after NS5ATP9 silencing or knockout. Results TAF/TDF significantly inhibited CCl 4 -induced liver fibrosis in mice, and regulated the differentiation, activation, and proliferation of hepatic stellate cells (HSCs). Furthermore, TAF/TDF suppressed the activities of TGFβ1/Smad3 and NF-κB/NLRP3 inflammasome signaling pathways in vivo and in vitro. NS5ATP9 inhibited liver fibrosis through TGFβ1/Smad3 and NF-κB signaling pathways. TAF/TDF upregulated the expression of NS5ATP9 in vivo and in vitro. Finally, TAF/TDF could only show marginal therapeutic effects when NS5ATP9 was silenced and knocked out in vivo and in vitro. Conclusions TAF/TDF prevented progression and promoted reversion of liver fibrosis through assembling TGFβ1/Smad3 and NF-κB/NLRP3 inflammasome signaling pathways via upregulating the expression of NS5ATP9. TAF/TDF also regulated the differentiation, activation, and proliferation of HSCs. The findings provided strong evidence for the role of TAF/TDF as a new promising therapeutic strategy in liver fibrosis.
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Frontiers in Endocrinology
·
2025
·
IF 4.6
Yuanfan Wu,Xia Sun,Yuhan Jia,Tianshu Gao,Jin Xu,Youqiao Qian,Naiqi Pei,Lilin Wang,Qiaohong Zheng,Honglei Li,Zhen Chen,Yijiao Liu,Yang Ma,Hui Chen,Yuanyuan Ye,Jiaxin Zhao,Yi Zhou,Xiaoqing Chen,Baosheng Huang,Yefeng Liu,Yin Zhu,Ning Xue,Juan Zhang,Guangfeng Ji,Xing Wang
This study aimed to evaluate the therapeutic effects of gigantol on hyperuricemia (HUA) and investigate the underlying mechanism of HUA. A mouse model of HUA was made by gavage of potassium oxonate, and HK-2 and AML12 cell models were made by adenosine and xanthine oxidase (XOD) induction. We tested the levels of uric acid (UA), creatinine (CRE), blood urea nitrogen (BUN), cellular UA, and XOD activity. The levels of NOD-like receptor thermal protein domain 3 (NLRP3) and other inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA) kits. XOD is a protein related to the NLRP3 pathway and also serves as an UA transporter. We found that the levels of UA, CRE, and BUN increased in serum but decreased in urine in HUA model mice. After gigantol treatment, UA, CRE, and BUN levels in serum decreased, whereas their levels in urine increased. The levels of NLRP3 and interleukin-1β (IL-1β) were lower and the expression of NLRP3-related protein decreased after gigantol treatment. In conclusion, gigantol exhibits a therapeutic effect on HUA, and the mechanism may be related to inhibiting XOD activity to reduce UA production, regulating the expression of UA transporters to increase UA excretion, and inhibiting the activation of NLRP3 inflammatory signaling.
研究领域:
药理学
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生物化学
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分子生物学
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免疫学
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PHYTOMEDICINE
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2024
·
IF 6.7
Miaomiao Sun,Honghong Zhan,Xiaoliang Long,Ali M. Alsayed,Zhe Wang,Fancheng Meng,Guowei Wang,Jingxin Mao,Zhihua Liao,Min Chen
Background Irinotecan (CPT-11) is used as chemotherapeutic drug for treatment of colorectal cancer. However, without satisfactory treatments, its gastrointestinal toxicities such as diarrhea and intestinal inflammation severely restrained its clinical application. Roots of Aucklandia lappa Decne. are used as traditional Chinese medicine to relieve gastrointestinal dysfunction and dehydrocostus lactone (DHL) is one of its main active components. Nevertheless, the efficacy and mechanism of DHL against intestinal mucositis remains unclear. Purpose The present study aimed to investigate the protective effects of DHL on CPT-11-induced intestinal mucositis and its underlying mechanisms. Methods The protective effect of DHL was investigated in CPT-11-induced mice and lipopolysaccharide (LPS)+CPT-11 induced THP-1 macrophages. Body weight, diarrhea score, survival rate, colon length, and histopathological changes in mice colon and jejunum were analyzed to evaluate the protective effect of DHL in vivo . And DHL on reducing inflammatory response and regulating TLR4/NF‐κB/NLRP3 pathway in vivo and in vitro were explored. Moreover, DHL on the interaction between TLR4 and MD2 was investigated. And silencing TLR4 targeted by siRNA was performed to validate the mechanisms of DHL on regulating the inflammation. Results DHL prevented CPT-11-induced intestinal damage, represented by reducing weight loss, diarrhea score, mortality rate and the shortening of the colon. Histological analysis confirmed that DHL prevented intestinal epithelial injury and improved the intestinal barrier function in CPT-11 induced mice. Besides, DHL significantly downregulated the level of inflammatory cytokines by inhibiting TLR4/NF-κB/NLRP3 signaling pathway in CPT-11-induced mice and LPS+CPT-11-induced THP-1 macrophages. In addition, DHL blocked TLR4/MD2 complex formation. Molecular docking combined with SIP and DARTS assay showed that DHL could bind to TLR4/MD2 and occludes the hydrophobic pocket of MD2. Furthermore, Silencing TLR4 abrogated the effect of DHL on LPS+CPT-11 induced inflammatory response in THP-1 macrophages. Additionally, DHL ameliorate the CPT-11-induced intestinal mucositis without affecting the anti-tumor efficacy of CPT-11 in the tumor xenograft mice. Conclusion This study found that DHL exhibited the anti-inflammatory effects in CPT-11-induced intestinal mucositis by inhibiting the formation of TLR4/MD2 complex and then regulation of NF-κB/NLRP3 signaling pathway. DHL is potentially served as a novel strategy of combined medication with CPT-11.
研究领域:
药理学
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免疫学
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肿瘤学
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胃肠病学
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2024
·Vol. 25
·期 16
·8878
·
IF 4.9
Lanfei Wang,Nianfeng Qiu,Suyuan Tong,Yan Yu,Shuhua Xi,Fei Wang
Arsenic (As) has been classified as a carcinogen for humans. There is abundant evidence indicating that arsenic increases the risk of bladder cancer among human populations. However, the underlying mechanisms have yet to be fully understood and elucidated. NADPH oxidases (NOXs) are the main enzymes for ROS production in the body. NADPH Oxidase 2 (NOX2), which is the most distinctive and ubiquitously expressed subunit of NOXs, can promote the formation and development of tumors. The utilization of NOX2 as a therapeutic target has been proposed to modulate diseases resulting from the activation of NOD-like receptor thermal protein domain associated protein 3 (NLRP3). Matrine has been reported to exhibit various pharmacological effects, including anti-inflammatory, antifibrotic, antitumor, and analgesic properties. However, it has not been reported whether matrine can inhibit malignant transformation induced by arsenic in uroepithelial cells through NOX2. We have conducted a series of experiments using both a sub-chronic NaAsO2exposure rat model and a long-term NaAsO2exposure cell model. Our findings indicate that arsenic significantly increases cell proliferation, migration, and angiogenesis in vivo and in vitro. Arsenic exposure resulted in an upregulation of reactive oxygen species (ROS), NOX2, and NLRP3 inflammasome expression. Remarkably, both in vivo and in vitro, the administration of matrine demonstrated a significant improvement in the detrimental impact of arsenic on bladder epithelial cells. This was evidenced by the downregulation of proliferation, migration, and angiogenesis, as well as the expression of the NOX2 and NLRP3 inflammasomes. Collectively, these findings indicate that matrine possesses the ability to reduce NOX2 levels and inhibit the transformation of bladder epithelial cells.
研究领域:
毒理学
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癌症研究
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药理学
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细胞生物学
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JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
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2024
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IF 5.7
Caihong Wang,Qihao Xu,Chaozhi Wei,Qinglian Hu,Yingping Xiao,Yuanxiang Jin
The higher prevalence of ulcerative colitis (UC) and the side effects of its therapeutic agents contribute to finding novel treatments. This study aimed to investigate whether kynurenine (KYN), a tryptophan metabolite, has the possibility of alleviating UC and further clarifying the underlying mechanism. The effect of KYN on treating UC was evaluated by intestinal pathology, inflammatory cytokines, and tight-junction proteins in colitis mice and LPS-stimulated Caco-2 cells. Our results revealed that KYN relieved pathological symptoms of UC, improved intestinal barrier function, enhanced AhR expression, and inhibited NF-κB signaling pathway activation in the colon of colitis mice. Moreover, the improved intestinal barrier function, the decreased inflammasome production, and the inhibited activation of the NF-κB signaling pathway by KYN were dependent on AhR in Caco-2 cells. KYN could trigger AhR activation, inactivate the NF-κB signaling pathway, and inhibit NLRP3 inflammasome production, thus alleviating intestinal epithelial barrier dysfunction and reducing intestinal inflammation. In conclusion, the present study reveals that KYN ameliorates UC by improving the intestinal epithelial barrier and activating the AhR-NF-κB-NLRP3 signaling pathway, and it can be a promising therapeutic agent and dietary supplement for alleviating UC.
研究领域:
胃肠病学
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免疫学
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药理学
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Journal of Translational Medicine
·
2025
·
IF 7.5
Liuzhu Chen,Linpei Zhuo,Jie Zheng,Xiaoyun Sun,Jing Sun,Jiaming Liu
Background Recent studies have highlighted the vital role of gut microbiota in the pathogenesis of Ischemic stroke (IS). However, the effects and underlying mechanisms of atorvastatin on IS via regulating gut-brain axis remain unclear. Thus, this study aimed to explore the relationship between atorvastatin, gut microbiota and IS through animal experiments, clinical trials and Mendelian randomization (MR) analysis. Methods Male mice were induced with bilateral common carotid artery occlusion (BCCAO) to establish an IS animal model, and then intragastrically treated with atorvastatin. Neurological deficits, microglia activation, and the levels of NLRP3 inflammasome and NF-κB pathway-related proteins were detected. Meanwhile, gut microbiota composition and intestinal barrier integrity were evaluated. In this prospective study, we recruited IS patients undergoing atorvastatin treatment, evaluated their functional outcomes, collected fecal samples, and assessed gut microbiota functions. Moreover, the causal relationships between specific bacteria, inflammation and IS were assessed via MR analysis. Results Our results showed that atorvastatin treatment significantly improved neurobehavioral deficits, suppressed activation of microglia, and inhibited NF-κB pathway as well as the formation of the NLRP3 inflammasome, reduced the release of inflammatory cytokines, including IL-1β and IL-18, which were reversed by antibiotics treatment. We further identified an increase in the genus Lachnospiraceae NK4A136 in atorvastatin-treated mice. Subsequent clinical experiments were conducted to explore the effects by analyzing the characteristic bacteria, such as Ruminococcus torques and Lachnospiraceae NK4A136 . The higher abundances of Ruminococcus torques and Lachnospiraceae NK4A136 were associated with a good outcome in atorvastatin-treated IS patients. MR analysis further revealed that these microbes were negatively correlated with inflammatory factor levels, and showed inhibitory effects on the Akt/NF-κB/NLRP3 pathway and PLA2G7 gene expression. Conclusion These findings demonstrated the roles of atorvastatin in regulating Akt/NF-κB/NLRP3 pathway to inhibit neuroinflammation through specific bacteria, which implied a novel way for IS treatment. Supplementary Information The online version contains supplementary material available at 10.1186/s12967-025-06803-w.
研究领域:
神经病学
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微生物学
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药理学
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免疫学
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JOURNAL OF NANOBIOTECHNOLOGY
·
2025
·Vol. 23
·期 1
·1-24
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IF 12.6
Tong Xin-Yi,Nong Wei-Jian,Tan Run-Min,Ouyang Jian-Ming
Objective This study aimed to compare the differences in pyroptosis and polarization of macrophages induced by different sizes of calcium oxalate monohydrate (COM) crystals and discuss the mechanism of kidney stone formation. Methods COM crystals with sizes of about 100 nm, 500 nm, 2.5 μm, and 10 μm were synthesized and characterized. THP-1 cells were induced to differentiate into macrophage-like cells. The damage of COM crystals to Mφs was evaluated by CCK-8 assay. The activation of the pyroptosis signaling pathway, cell morphology, and proportion of pyroptosis cells in Mφs induced by COM crystals were detected. Finally, the proportion of M1/M2 polarization was qualitatively and quantitatively assessed. Results COM-100 nm, COM-500 nm, COM-2.5 μm, and COM-10 μm all significantly induced the pyroptosis and polarization of Mφs. Among them, at the same cell viability, COM-10 μm induced the highest pyroptosis rate. The expression of NLRP3 and GSDMD-N induced by COM-10 μm increased by 81.43 ± 11.45% and 112.00 ± 9.87%, respectively, and the rate of caspase-1/PI double-positive pyroptosis cells was 22.2%. Meanwhile, COM-10 μm induced the highest proportion of M1 polarization (M1/M2 ratio was 209.90% ± 2.54%). Conclusion COM-10 μm significantly activates the classical caspase-1-mediated pyroptosis pathway and promotes M1 polarization in Mφs. Therefore, at the same cell viability, large-sized micro-COM is more capable of inducing inflammation than nano-COM. Graphical
研究领域:
纳米技术
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泌尿科学
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免疫学
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细胞生物学
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材料科学
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