JOURNAL OF ETHNOPHARMACOLOGY
·
2019
·
IF 3.414
Yanbei Tu,Kai Wang,Yeer Liang,Xuejing Jia,Lili Wang,Jian-Bo Wan,Jianping Han,Chengwei He
Ethnopharmacological relevance The whole plant of Glycine tabacina (Labill.) Benth has been used as a traditional herbal medicine to treat rheumatism , ostealgia and nephritis in China. It is also one of the sources of the renowned native herbal medicine ‘I-Tiao-Gung’ in Taiwan. Aim of the study This study aimed to investigate the anti-arthritic effect of ethanol extract of G. tabacina (GTE) in a collagen-induced arthritis (CIA) rat model. Materials and methods The chemical profile of GTE was analyzed by HPLC-UV. The CIA was induced in male Wistar rats by intradermal injection of bovine type II collagen at tail root, back and ankle joints. The rats were orally administrated daily with GTE (1.11, 2.22 and 4.44 g dry weight of herb powder per kg body weight) from day 0 and continued for 30 days. Swelling volume and thickness of paw, arthritis index, X-radiographs and histopathological changes were examined to assess the severity of arthritis. Furthermore, the levels of pro-inflammatory cytokines, such as interleukin1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α), total superoxide dismutase (T-SOD) activity and malonaldehyde (MDA) level were measured to preliminarily explore the possible mechanisms. Results Oral administration of GTE significantly ameliorated the arthritic symptoms in CIA rat model, as indicated by the effects on paws swelling and arthritis index. X-radiographic analysis and histopathological examinations demonstrated that GTE effectively protected the bone and cartilage of joints from erosion, lesion and deformation. The efficacy of GTE treatment on CIA was comparable to that of indomethacin (positive drug). Besides, the overproduction of IL-1β, IL-6 and TNF-α was remarkably inhibited in the serum of all GTE treatment groups. The restoration of serum T-SOD activity and MDA level proved that GTE administration alleviated the oxidative stress in CIA rats. Conclusions GTE exhibited strong anti-CIA activity through inhibiting pro-inflammatory cytokines and oxidation in rats, suggesting its potential preventive and therapeutic effects on rheumatoid arthritis (RA).
研究领域:
药理学
·
民族药理学
·
免疫学
·
风湿病学
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产品关联
DOI
PubMed
高影响因子
Experimental and Therapeutic Medicine
·
2022
·Vol. 24
·期 6
·1-8
·
IF 2.751
Na Ren,Shanshan Shi,Na Zhao,Lingyan Zhang
Dual specificity phosphatase 22 (DUSP22) regulates fibrosis and inflammation, which may be implicated in the development of diabetic nephropathy (DN). Hence, the current study aimed to assess the effect of DUSP22 on cell proliferation, apoptosis, fibrosis and inflammation in mouse mesangial cell line (SV40‑MES13) under both high glucose (HG) and low glucose (LG) conditions. SV40‑MES13 cells were treated with HG and LG, then HG‑group cells were transfected with DUSP22 overexpression and control plasmids, meanwhile LG‑group cells were transfected with DUSP22 and control siRNAs. Then, cell proliferation using Cell Counting Kit‑8, cell apoptosis by TUNEL assay, protein expression using western blotting, inflammatory cytokines using ELISA and RNA using reverse transcription‑quantitative PCR were determined. DUSP22 mRNA and protein were decreased in SV40‑MES13 cells under the HG condition compared with those under the LG condition. Under the HG condition, DUSP22 overexpression suppressed SV40‑MES13 cell proliferation at 48 and 72 h as well as Bcl2, but it facilitated TUNEL‑reflected apoptotic rate and cleaved‑caspase‑3; besides, DUSP22 overexpression restrained proteins of fibronectin 1, collagen I, transforming growth factor beta 1, and their corresponding mRNAs. As to the inflammation, DUSP22 overexpression downregulated TNF‑α, IL‑1β, IL‑6 and IL‑12 under the HG condition. By contrast, DUSP22 siRNA promoted SV40‑MES13 cell proliferation, fibrosis and inflammation, but attenuated apoptosis in SV40‑MES13 cells under the LG condition. Additionally, DUSP22 overexpression inactivated phosphorylated (p)‑ERK, p‑JNK, and p‑P38 in HG‑treated SV40‑MES13 cells; differently, DUSP22 small interfering RNA facilitated them under the LG condition. In conclusion, DUSP22 suppresses HG‑induced mesangial cell hyperproliferation, fibrosis, inflammation and the MAPK pathway, implying its potency in DN treatment.
研究领域:
分子生物学
·
细胞生物学
·
糖尿病研究
·
肾病学
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产品关联
DOI
PubMed
高影响因子
Food Bioscience
·
2023
·
IF 5.2
Shuna Chen,Jiaxin Kang,Huanqing Zhu,Ziyi Han,Leyu Wang,Kaixi Wang,Junsheng Liu,Yuanyuan Wu,Puming He,Youying Tu,Bo Li
The impacts of tea seed saponins (TSS) on intestinal injury, immune disorder, gut microbial dysbiosis and serum metabolome in cyclophosphamide (CTX)-induced mice were explored. The findings indicated that TSS significantly reversed the spleen index, protected intestinal mucosa , and increased the protein levels of tumor necrosis factor-α (TNF-α), occludin , interleukin-6 (IL-6) and immunoglobulin A (IgA) in colon and small intestine of mice. Microbiome analysis suggested that TSS shaped the gut microbial community structure, and mainly increased the proportion of Bacillus and Alloprevotella . The in vitro experiment further demonstrated the ability of TSS to promote the growth of Bacillus . Serum metabolome analysis showed that TSS significantly upregulated and downregulated 18 and 15 metabolites, respectively. Eight of these compounds were correlated with Bacillus and Alloprevotella . Over all, this work demonstrated that TSS could improve CTX-induced immune imbalance, intestinal barrier disruption and gut microbial dysbiosis, and was a potential candidate for regulating intestinal homeostasis .
研究领域:
药理学
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免疫学
·
微生物学
·
代谢组学
·
胃肠病学
✓ 已验证
产品关联
DOI
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2023
·
IF 6.8
Cheng-Qiang Wang,Zou Su,Chun-Guang Dai,Jia-Le Song,Bo Qian
2,2′,4,4′-tetrabromodiphenyl ether (BDE47) is a foodborne environmental risk factor for depression, but the pathogenic mechanism has yet to be fully characterized. In this study, we clarified the effect of BDE47 on depression in mice. The abnormal regulation of the microbiome-gut-brain axis is evidenced closely associated with the development of depression. Using RNA sequencing, metabolomics, and 16s rDNA amplicon sequencing, the role of the microbiome-gut-brain axis in depression was also explored. The results showed that BDE47 exposure increased depression-like behaviors in mice but inhibited the learning memory ability of mice. The RNA sequencing analysis showed that BDE47 exposure disrupted dopamine transmission in the brain of mice. Meanwhile, BDE47 exposure reduced protein levels of tyrosine hydroxylase (TH) and dopamine transporter (DAT), activated astrocytes and microglia cells, and increased protein levels of NLRP3, IL-6, IL-1β, and TNF-α in the brain of mice. The 16 s rDNA sequencing analysis showed that BDE47 exposure disrupted microbiota communities in the intestinal contents of mice, and faecalibaculum was the most increased genus. Moreover, BDE47 exposure increased the levels of IL-6, IL-1β, and TNF-α in the colon and serum of mice but decreased the levels of tight junction protein ZO-1 and Occludin in the colon and brain of mice. In addition, the metabolomic analysis revealed that BDE47 exposure induced metabolic disorders of arachidonic acid and neurotransmitter 2-Arachidonoyl glycerol (2-AG) was one of the most decreased metabolites. Correlation analysis further revealed gut microbial dysbiosis, particularly faecalibaculum , is associated with altered gut metabolites and serum cytokines in response to BDE47 exposure. Our results suggest that BDE47 might induce depression-like behavior in mice through gut microbial dysbiosis. The mechanism might be associated with the inhibited 2-AG signaling and increased inflammatory signaling in the gut-brain axis.
研究领域:
神经科学
·
药理学
·
分子生物学
·
微生物学
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免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
MOLECULES
·
2024
·Vol. 29
·期 9
·2076
·
IF 4.2
Ruiding Wen,Lu Luo,Runcheng Zhang,Xudong Zhou,Wei Wang,Limin Gong
A neutralPolygonatumcyrtonemapolysaccharide (NPCP) was isolated and purified fromPolygonatumcyrtonemaby various chromatographic techniques, including DEAE-52 and Sephadex-G100 chromatography. The structure of NPCP was characterized by HPLC, HPGPC, GC-MS, FT-IR, NMR, and SEM. Results showed that NPCP is composed of glucose (55.4%) and galactose (44.6%) with a molecular weight of 3.2 kDa, and the sugar chain of NPCP was →1)-α-D-Glc-(4→1)-β-D-Gal-(3→. In vitro bioactivity experiments demonstrated that NPCP significantly enhanced macrophages proliferation and phagocytosis while inhibiting the M1 polarization induced by LPS as well as the M2 polarization induced by IL-4 and IL-13 in macrophages. Additionally, NPCP suppressed the secretion of IL-6 and TNF-α in both M1 and M2 cells but promoted the secretion of IL-10. These results suggest that NPCP could serve as an immunomodulatory agent with potential applications in anti-inflammatory therapy.
研究领域:
药理学
·
免疫学
·
生物化学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
·
2015
·
IF 2.084
Juanli Fu,Qiong Shi,Xiufang Song,Xiaomin Xia,Chuanyang Su,Zixuan Liu,Erqun Song,Yang Song
Tetrachlorobenzoquinone (TCBQ) is a joint metabolite of persistent organic pollutants (POPs), hexachlorobenzene (HCB) and pentachlorophenol (PCP). Previous studies have been reported that TCBQ contributes to acute hepatic damage due to its pro-oxidative nature. In the current study, TCBQ showed the highest capacity on the cytotoxicity, ROS formation and inflammatory cytokines release among four compounds, i.e., HCB, PCP, tetrachlorohydroquinone (TCHQ, reduced form of TCBQ) and TCBQ, in PC 12 cells. Further mechanistic study illustrated TCBQ activates nuclear factor-kappa B (NF-κB) signaling. The activation of NF-κB was identified by measuring the protein expressions of inhibitor of nuclear factor kappa-B kinase (IKK) α/β, p-IKKα/β, an inhibitor of NF-κB (IκB) α, p-IκBα, NF-κB (p65) and p-p65. The translocation of NF-κB was assessed by Western blotting of p65 in nuclear/cytosolic fractions, electrophoretic mobility shift assay (EMSA) and luciferase reporter gene assay. In addition, TCBQ significantly induced protein and mRNA expressions of inflammatory cytokines and mediators, such as interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and the production of nitric oxide (NO) and prostaglandin E2 (PGE2). Pyrrolidine dithiocarbamate (PDTC), a specific NF-κB inhibitor inhibited these effects efficiently, further suggested TCBQ-induced inflammatory responses involve NF-κB signaling. Moreover, antioxidants, i.e., N-acetyl- l -cysteine (NAC), Vitamin E and curcumin, ameliorated TCBQ-induced ROS generation as well as the activation of NF-κB, which implied that ROS serve as the upstream molecule of NF-κB signaling. In summary, TCBQ exhibits a neurotoxic effect by inducing oxidative stress-mediated inflammatory responses via the activation of IKK/IκB/NF-κB pathway in PC12 cells.
研究领域:
毒理学
·
神经科学
·
细胞生物学
·
药理学
✓ 已验证
DOI
PubMed
高影响因子
Bioengineered
·
2022
·
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.
研究领域:
免疫学
·
细胞生物学
·
分子生物学
·
妇科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Food & Function
·
2022
·Vol. 13
·期 16
·8593-8604
·
IF 6.317
Yanfang Yu,Yuhuan Chen,Xuping Shi,Chuan Ye,Junwen Wang,Jinzhi Huang,Bing Zhang,Zeyuan Deng
This study investigated the hepatoprotective effects of various mulberry (Morus alba L.) leaf extracts (MLEs), including mulberry ethanol extract (MEE), aqueous extract (MAE) and a combination extract (MCE) against D-galactosamine (D-GalN)/lipopolysaccharide (LPS)-induced acute liver injury in rats. It aimed to explore the possible molecular mechanism of the liver-protecting function of mulberry leaves and provide a reference for choosing the appropriate extraction method. The results showed that the three extracts contained different amounts of phenolic compounds, 1-deoxynojirimycin (DNJ) and polysaccharides. MLEs markedly improved the pathological status of rat liver tissue, decreased the levels of AST, ALT, TNF-α, IL-1β, IL-6 and MDA, while increased the levels of GSH, SOD and CAT in the D-GalN/LPS-treated rats at the same time. MEE, with the highest amount of total phenolics, exhibited the highest antioxidant activity corresponding to the protein expression level of Nrf2 and HO-1. MCE significantly suppressed the expression of apoptosis-related dot-like protein (ASC) and Caspase-1 and inhibited the phosphorylation of p38 MAPK and ERK1/2, thereby showing high anti-inflammatory activity. These results indicated that the active components from mulberry leaves protected rats against acute liver injury, attributed to a reduction in both oxidative stress and inflammatory response. The protective effect may be implicated in regulating the Nrf2, NLRP3 and MAPK signaling pathways.
研究领域:
药理学
·
肝病学
·
生物化学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CNS Neuroscience & Therapeutics
·
2023
·Vol. 29
·期 4
·1000-1011
·
IF 5.5
Di Zhang,Bei Jing,Zhen-ni Chen,Xin Li,Hui-mei Shi,Ya-chun Zheng,Shi-quan Chang,Li Gao,Guo-ping Zhao
Introduction Sciatica causes intense pain. No satisfactory therapeutic drugs exist to treat sciatica. This study aimed to probe the potential mechanism of ferulic acid in sciatica treatment. Methods Thirty-two SD rats were randomly divided into 4 groups: sham operation, chronic constriction injury (CCI), mecobalamin, and ferulic acid. We conducted RNA sequencing, behavioral tests, ELISA, PCR, western blotting, and immunofluorescence analysis. TAK-242 and JSH23 were administered to RSC96 and GMI-R1 cells to explore whether ferulic acid can inhibit apoptosis and alleviate inflammation. Results RNA sequencing showed that TLR4/NF-κB pathway is involved in the mechanism of sciatica. CCI induced cold and mechanical hyperalgesia; destroyed the sciatic nerve structure; increased IL-1β, IL-6, TNF-α, IL-8, and TGF-β protein levels and IL-1β, IL-6, TNF-α, TGF-β, TLR4, and IBA-1 mRNA levels; and decreased IL-10 and INF-γ protein levels and IL-4 mRNA levels. Immunohistochemistry showed that IBA-1, CD32, IL-1β, iNOS, nNOS, COX2, and TLR4 expression was increased while S100β and Arg-1 decreased. CCI increased TLR4, IBA-1, IL-1β, iNOS, Myd88, p-NF-κB, and p-p38MAPK protein levels. Treatment with mecobalamin and ferulic acid reversed these trends. Lipopolysaccharide (LPS) induced RSC96 cell apoptosis by reducing Bcl-2 and Bcl-xl protein and mRNA levels and increasing Bax and Bad mRNA and IL-1β, TLR4, Myd88, p-NF-κB, and p-p38MAPK protein levels, while ferulic acid inhibited cell apoptosis by decreasing IL-1β, TLR4, Myd88, p-NF-κB, and p-p38MAPK levels and increasing Bcl-2 and Bcl-xl levels. In GMI-R1 cells, Ferulic acid attenuated LPS-induced M1 polarization by decreasing the M1 polarization markers IL-1β, IL-6, iNOS, and CD32 and increasing the M2 polarization markers CD206, IL-4, IL-10 and Arg-1. After LPS treatment, IL-1β, iNOS, TLR4, Myd88, p-p38MAPK, and p-NF-κB levels were obviously increased, and Arg-1 expression was reduced, while ferulic acid reversed these changes. Conclusion Ferulic acid can promote injured sciatic nerve repair by reducing neuronal cell apoptosis and inflammatory infiltration though the TLR4/NF-κB pathway.
研究领域:
神经科学
·
药理学
·
分子生物学
·
细胞生物学
·
炎症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Small
·
2024
·
IF 13
Ya Wang,Yujie Zhang,Pengqian Wang,Jing Han,Xiaojiang Zhang,Feiyu Shi,Zhe Zhang,Gang Guo,Ruochen Wang,Dan Shao,Daocheng Wu,Junjun She
Inspired by the timely emergence of silkworm pupae from their cocoons, silkworm chrysalis-like probiotic composites (SCPCs) are developed for the comprehensive therapy of inflammatory bowel disease (IBD), in which probiotics are enveloped as the “pupa” in a sequential layering of silk sericin (SS), tannic acid (TA), and polydopamine, akin to the protective “cocoon”. Compared to unwrapped probiotics, these composites not only demonstrate exceptional resistance to the harsh gastrointestinal environment and exhibit over 200 times greater intestinal colonization but also safeguard probiotics from the damage of IBD environment while enabling probiotics sustained release. The probiotics, in synergy with SS and TA, provide a multi-crossed comprehensive therapy for IBD that simultaneously addresses various pathological features of IBD, including intestinal barrier disruption, elevated pro-inflammatory cytokines, heightened oxidative stress, and disturbances in the intestinal microbiota. SCPCs exhibit remarkable outcomes, including a 9.7-fold reduction in intestinal permeability, an 8.9-fold decrease in IL-6 levels, and a 2.9-fold reduction in TNF-α levels compared to uncoated probiotics. Furthermore, SCPCs demonstrate an impressive 92.25% reactive oxygen species clearance rate, significantly enhance the richness of beneficial intestinal probiotics, and effectively diminish the abundance of pathogenic bacteria, indicating a substantial improvement in the overall therapeutic effect of IBD.
研究领域:
生物医学工程
·
药学
·
胃肠病学
·
微生物学
·
材料科学
✓ 已验证
DOI
PubMed
高影响因子
FOOD CHEMISTRY
·
2025
·
IF 9.8
Jiao Wu,Xiang-Tan Xu,Cheng Xing,Xin-Bao Hao,Xing-Yue Fang,Zhi-Hao Xie,Shan Zhao,Jing-Lin Gao,Lu Xu,Shi-Jie Wang
Honey has been recognized for its role in disease prevention through nutritional modulation. In this study, we comprehensively assessed the physicochemical parameters, metabolic profile, antioxidant and anti-inflammatory activities of multifloral honeys produced by Apis cerana cerana in Sansha City (SS), Hainan Province. Metabolomic analysis identified SS honey had multiple bioactive compounds known for antioxidant and anti-inflammatory properties. Compared to A. cerana cerana honey from central regions of Hainan Province, SS honey showed higher levels of TFC (113.80 mg RE/100 g) and TPC (45.86 mg GAE/100 g). Furthermore, SS honey demonstrated greater antioxidant activity, as evidenced by FRAP (1503.16 μmol TE/kg), DPPH IC 50 (36.13 mg/mL), and ABTS IC 50 (11.03 mg/mL). SS honey significantly reduced the levels of cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), and tumor necrosis factor-α (TNF-α) in lipopolysaccharide (LPS)-induced RAW 264.7 cells, along with suppressing the mRNA expression of these inflammatory markers.
研究领域:
养蜂学
·
生物化学
·
药理学
·
营养科学
·
代谢组学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Acta Biomaterialia
·
2021
·
IF 8.947
Shikun Wei,Pengcheng Xu,Zexin Yao,Xiao Cui,Xiaoxuan Lei,Linlin Li,Yunqing Dong,Weidong Zhu,Rui Guo,Biao Cheng
Diabetic wound healing remains a major challenge due to its vulnerability to bacterial infection, as well as the less vascularization and prolonged inflammatory phase. In this study, we developed a hydrogel system for the treatment of chronic infected wounds, which can regulate inflammatory (through the use of antimicrobial peptides) and enhance collagen deposition and angiogenesis (through the addition of platelet-rich plasma (PRP)). Based on the formation of Schiff base linkage, the ODEX/HA-AMP/PRP hydrogel was prepared by mixing oxidized dextran (ODEX), antimicrobial peptide-modified hyaluronic acid (HA-AMP) and PRP under physiological conditions, which exhibited obvious inhibition zones against three pathogenic bacterial strains ( E. coli, S. aureus and P. aeruginosa ) and slow release ability of antimicrobials and growth factors. Moreover, CCK-8, live/dead fluorescent staining and scratch test confirmed that ODEX/HA-AMP/PRP hydrogel could facilitate the proliferation and migration of L929 fibroblast cells. More importantly, in vivo experiments further demonstrated that the prepared hydrogels could significantly improve wound healing in a diabetic mouse infection by regulating inflammation, accelerating collagen deposition and angiogenesis. In addition, prepared hydrogel showed a significant antibacterial activity against S. aureus and P. aeruginosa, inhibited pro-inflammatory factors (TNF-α, IL-1β and IL-6), enhanced anti-inflammatory factors (TGF-β1) and vascular endothelial growth factor (VEGF) production. The findings of this study suggested that the composite hydrogel with AMP and PRP controlled release ability could be used as a promising candidate for chronic wound healing and infection-related wound healing.
研究领域:
生物医学工程
·
药学
·
伤口愈合
·
糖尿病研究
·
传染病学
✓ 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）