PROCESS BIOCHEMISTRY
·
2022
·
IF 4.885
Yanyan Qian,Li Wang,Zhiqiang Zhang,Xinxin Li,Chaofei Niu,Xiao Li,Erjuan Ning,Bingji Ma
The crude heteropolysaccharides from four forms of Rehmannia glutinosa were extracted by boiling water, then purified and named FRP, DRP, HRP and NRP, respectively. The physicochemical properties, blood-enriching and immunomodulatory activities of the heteropolysaccharides were analyzed. Mg, Ca and K were the dominant metal elements in all four fractions; galactose and galacturonic acid were the predominant monosaccharides . All fractions had good thermal stabilities . The bioactive tests showed that the levels of HCT and HGB in all four groups were significantly higher than that in the model group. In addition, FRP, DRP, HRP and NRP can significantly stimulate mRNA levels of tumor necrosis factor- α (TNF- α ), interleukin-6 (IL-6), interleukin-4 (IL-4), and interleukin-10 (IL-10). The immunomodulatory activities of HRP and NRP were better than that of DRP and FRP, while immunomodulatory activities of HRP were better than that of NRP. The results demonstrated that the heteropolysaccharides from different R. glutinosa products can improve blood-enriching activities and immunomodulatory activities. These results provide experimental evidence to justify further research of heteropolysaccharides from R. glutinosa in pharmaceuticals and functional foods.
研究领域:
药理学
·
免疫学
·
生物化学
✓ 已验证
产品关联
DOI
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2017
·
IF 2.956
Zhaoxiao Yu,Chenhui Zhang,Mingliang Zhou,Qiming Li,Hui Li,Wei Duan,Xue Li,Yonghong Feng,Jianping Xie
Tuberculosis (TB), caused by Mycobacterium tuberculosis , remains a formidable threat to global public health . The successful intracellular persistence of M . tuberculosis significantly contributes to the intractability of tuberculosis. Proline-glutamic acid (PE) and proline-proline-glutamic acid (PPE) are mycobacterial exclusive protein families that widely reported to be involved in the bacterial virulence , physiology and interaction with host. Rv2770c (PPE44), a predicted virulence factor , was up-regulated upon the infected guinea pig lungs. To investigate the role of Rv2770c, we heterologously expressed the PPE44 in the nonpathogenic fast-growing M . smegmatis strain. Subcellular location analysis demonstrated that Rv2770c is a cell wall associated protein, suggestive of a potential candidate involved in host-pathogen interaction. The Rv2770c can enhance M . smegmatis survival within macrophages and under stresses such as H 2 O 2 , SDS, diamide exposure, and low pH condition. M . smegmatis expressing Rv2770c is more virulent as testified by the increased death of macrophages and the increased expression of interlukin-6 (IL-6) and interlukin-12p40 (IL-12p40). Moreover, Rv2770c altered the secretion of IL-6 and IL-12p40 of macrophages via NF-κB, ERK1/2 and p38 MAPK axis. Taken together, this study implicated that Rv2770c was a virulent factor actively engaged in the interaction with host macrophage.
研究领域:
微生物学
·
免疫学
·
分子生物学
✓ 已验证
DOI
高影响因子
MICROCHIMICA ACTA
·
2024
·Vol. 191
·期 11
·1-11
·
IF 5.3
Huang Yong,Chen Miao,Jiang Fengjuan,Lu Chengzhe,Zhu Qunshan,Yang Yan,Fu Lei,Li Limao,Liu Jia,Wang Zhenguang,Cao Xiaowei,Wei Wei
Studies have found that matrix metalloproteinase-9 (MMP-9) and interleukin-6 (IL-6) play an important role in tumorigenesis. In order to detect MMP-9 and IL-6 concentrations with high sensitivity and specificity, an efficient microfluidic-SERS sensing system was prepared based on surface-enhanced Raman scattering (SERS). The aptamer recognition-release mechanism and the dual signal amplification strategy were applied in the sensing system. The sensor system was developed using two kinds of nanomaterials with excellent SERS properties, namely gold-coated iron tetroxide particles (Fe 3 O 4 @AuNPs) and gold nanocages (AuNCs). In addition, Fe 3 O 4 @AuNPs also has magnetic adsorption properties. In the sensing system, single-stranded DNA1 (ssDNA1) and aptamer were modified on Fe 3 O 4 @AuNPs. Single-stranded DNA2 (ssDNA2) and Raman tags were modified on AuNCs. When the target was present, the aptamer bound to the target and detached from the Fe 3 O 4 @AuNPs, and ssDNA2 bound to the exposed ssDNA1. At this time, the Fe 3 O 4 @AuNPs@AuNCs@SERS tag complex was formed, and the SERS signal was enhanced for the first time. Under the action of an external magnet on the microfluidic chip, the complex was magnetized and enriched. The SERS signal was enhanced for the second time. Due to the high affinity between the aptamer and the target object, the sensing system has a strong specificity. The double amplification of the SERS signal gave the system excellent sensitivity. The limit of detection (LOD) relative to MMP-9 and IL-6 were as low as 0.178 pg/mL and 0.165 pg/mL, respectively. The microfluidic-SERS sensing system has a feasible prospect in the early screening of gastric cancer. Graphical
研究领域:
生物医学工程
·
分析化学
·
癌症研究
·
纳米技术
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
·
IF 4.8
Shu-Zhen Dai,Ri-Hong Wu,Hengyu Chen,Ming-Hui Chen,Weijing Xie,Wu-Ping Zheng,Guang-Hong Tan,Feng-Ying Huang
Background The process of NETosis is observed in a range of inflammatory conditions. Progesterone (P4) has been shown to alleviate inflammation caused by viral infections such as influenza and SARS-CoV-2. However, the precise molecular mechanisms responsible for this effect are not yet fully understood. Therefore, the present investigation aims to explore whether P4 can exert its anti-inflammatory properties by inhibiting NETosis and the related molecular pathways. Methods Airway inflammation caused by rhinovirus serotype-1b (RV-1b) was induced in male BALB/c mice. The inflammation was assessed through histological examination and calculation of inflammatory cells present in the bronchoalveolar lavage fluid. Flow cytometry was used to analyze the inflammatory cells and NETotic neutrophils. Western blotting analysis was conducted to detect proteins associated with NETosis, inflammasome activation, and signaling. Furthermore, confocal microscopy was utilized to observe neutrophil extracellular trap (NET) structures in vivo tissues and in vitro neutrophils, neutrophil infiltration, and inflammasome formation. Results The administration of P4 proved to be an effective treatment for reducing airway inflammation and the production of NETs caused by RV-1b infection. The infection triggered the activation of NLRP3 inflammasomes in neutrophils, which led to the maturation of IL-1β and subsequent activation of both the NF-κB and p38 signaling pathways. The activation of NF-κB signaling resulted in the secretion of downstream chemokines CCL3 and IL-6, which led to an increase in neutrophil infiltration into the lung airways. Moreover, the activation of p38 signaling led to the generation of reactive oxygen species, resulting in NETosis. However, the administration of P4 inhibited the activation of the NLRP3 inflammasome, which subsequently led to the deactivation of both the IL-1β-NF-κB and IL-1β-p38 axes. As a result, there was a reduction in neutrophil infiltration and NETosis. Furthermore, TGF-β-activated kinase 1 (TAK1) was identified as an intermediary enzyme. P4 inhibits both the NF-κB and IL-1β-p38 pathways by suppressing the activity of TAK1. Conclusion The capacity of P4 to mitigate rhinovirus-induced airway inflammation is attributed to its ability to impede the infiltration of neutrophils and NETosis. As inflammation mediated by NETosis is widespread in diverse disorders, our findings propose that P4 could potentially function as a universal therapeutic agent in the management of such ailments.
研究领域:
免疫学
·
呼吸病学
·
病毒学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Animal Models and Experimental Medicine
·
2024
·
IF 3.8
Bing Zhang,Tingting Fu,Yi Han,Gongke Li,Xianyao Wan,Yong Li
Backgroud Thoracic Trauma and Limb Fractures Are the Two most Common Injuries in Multiple Trauma. However, there Is Still a Lack of Mouse Models of Trauma Combining Tibial Shaft Fracture (TSF) and Thoracic Trauma. In this Study, we Attempted to Develop a Novel Mouse Model of TSF Combined with Blunt Chest Trauma (BCT). Methods A total of 84 C57BL/6J male mice were used as the multiple trauma model. BCT was induced by hitting the chests of mice with heavy objects, and TSF was induced by hitting the tibia of mice with heavy objects after intramedullary fixation. Serum specimens of mice were received by cardiac puncture at defined time points of 0, 6, 12, 24, 48, and 72 h. Results Body weight and body temperature tended to decrease within 24 h after multiple trauma. Hemoglobin analyses revealed a decrease during the first 24 h after multiple trauma. Some animals died by cardiac puncture immediately after chest trauma. These animals exhibited the most severe pulmonary contusion and hemorrhage. The level of lung damage varied in diverse mice but was apparent in all animals. Classic hematoxylin and eosin (H&E)-stained paraffin pulmonary sections of mice with multiple trauma displayed hemorrhage and an immunoinflammatory reaction. Bronchoalveolar lavage fluid (BALF) and serum samples of mice with multiple trauma showed an upregulation of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-1 α (TNF-1 α ) compared with the control group. Microimaging confirmed the presence of a tibia fracture and pulmonary contusion. Conclusions The novel mouse multiple trauma model established in this study is a common trauma model that shows similar pathological mechanisms and imaging characteristics in patients with multiple injuries. This study is useful for determining whether blockade or intervention of the cytokine response is beneficial for the treatment of patients with multiple trauma. Further research is needed in the future.
研究领域:
创伤外科
·
免疫学
·
病理学
✓ 已验证
DOI
PubMed
高影响因子
American Journal of Translational Research
·
2018
·
IF 3.061
Qin Zhu,Peifen Zheng,Xinyu Chen,Feng Zhou,Qiaona He,Yuefeng Yang
Ulcerative colitis (UC) is a chronic and nonspecific intestinal inflammatory disease, which may increase the risk of colon cancer. Andrographolide is a main active component of Andrographis paniculata . The anti-inflammatory ability of andrographolide suggested its potential therapeutic effect against UC. In the present study, elevated serum concentrations of proinflammatory factors, including (TNF)-α, interleukin (IL)-1β, IL-6 and IL-23, as well as increased percentages of Th17 cells (IL-17+CD4+ cells) in CD4+ cells were detected in UC patients compared to that in healthy donors. These data suggested that Th17 immune responses may involve in the pathogenesis of UC. Experimental colitis mouse model was then established. The results of hematoxylin and eosin staining demonstrated the therapeutic effect of andrographolide on colitis. Enzyme-linked immunosorbent assay (ELISA), flow cytometry and western blotting analyses showed that andrographolide could decreased the levels of proinflammatory factors TNF-α, IL-1β, IL-6 and IL-17A in the serum and in the colon tissues, reduced the percentages of Th17 cells in CD4+ cells, and suppressed the levels of IL-23, IL-17A, ROR-γt (key transcription factor of Th17 cells) and p-STAT3 in the colon tissues. Further, peripheral blood mononuclear cells (PBMCs) were isolated from UC patients and treated with various concentrations of andrographolide (0, 10, 20 and 30 μg/ml). Andrographolide also showed inhibitory effects on the levels of proinflammatory factors, the percentages of Th17 cells and the expression of relative proteins. Similar results were obtained in lipopolysaccharide-treated normal PBMCs. These data suggested that andrographolide may inhibit Th17 immune response via STAT3 signaling. In conclusion, we demonstrated that andrographolide inhibited the activity of IL-23/IL-17 axis and down-stream pro-inflammatory factors so as to suppress inflammation response, resulting in the relieving of UC.
研究领域:
免疫学
·
药理学
·
炎症性肠病
✓ 已验证
DOI
PubMed
高影响因子
Research
·
2022
·
IF 11.036
Yanhong Wang,Fangchao Xue,Yanzhao Li,Lin Lin,Yeqin Wang,Shanlan Zhao,Xingli Zhao,Yong Liu,Ju Tan,Gang Li,Haoran Xiao,Juan Yan,Hao Tian,Min Liu,Qiao Zhang,Zhaojing Ba,Lang He,Wenyan Zhao,Chuhong Zhu,Wen Zeng
Rapid integration into the host tissue is critical for long-term patency after small diameter tissue engineering vascular grafts (sdTEVGs) transplantation. Neural recognition may be required for host integration and functionalization of the graft. However, immune rejection and inflammation hinder nerve regeneration of sdTEVGs. Here, a CRISPR/dCas9-nanocarrier was used for targeted programming of regulatory T cells (Treg cells) in situ to promote nerve regeneration of sdTEVGs by preventing excessive inflammation. Treg cells and (C-C chemokine receptor) CCR2+ macrophage recruitment occurred after transplantation. The nanodelivery system upregulated ten eleven translocation (TET2) in Treg cells in vitro. Reprogrammed Treg cells upregulated anti-inflammatory cytokines and decreased the proportion of CCR2+ macrophages. IL-6 concentrations decreased to the levels required for nerve regeneration. Implantation of CRISPR/dCas9 nanodelivery system-modified sdTEVGs in rats resulted in Treg cell editing, control of excessive inflammation, and promoted nerve regeneration. After 3 months, nerve regeneration was similar to that observed in normal blood vessels; good immune homeostasis, consistency of hemodynamics, and matrix regeneration were observed. Neural recognition promotes further integration of the graft into the host, with unobstructed blood vessels without intimal hyperplasia. Our findings provide new insights into vascular implant functionalization by the host.
研究领域:
生物医学工程
·
免疫学
·
组织工程
·
分子生物学
·
纳米技术
✓ 已验证
DOI
PubMed
高影响因子
Scientific Reports
·
2018
·Vol. 8
·期 1
·1-11
·
IF 4.122
Li Lili,Zhang Sheng,Xin Yanfei,Sun Junying,Xie Feng,Yang Lin,Chen Zhiqin,Chen Hao,Liu Fang,Xuan Yaoxian,You Zhenqiang
Quzhou Fructus Aurantii (QFA) is an authentic herb of local varieties in Zhejiang, China, which is usually used to treat gastrointestinal illnesses, but its effects on respiratory inflammation have not been reported yet. In our study, the anti-inflammatory activity of QFA extract (QFAE) was evaluated on copper sulfate pentahydrate (CuSO 4 ·5H 2 O)-induced transgenic neutrophil fluorescent zebrafish model. QFAE showed a significant effect of anti-inflammation in CuSO 4 ·5H 2 O-induced zebrafish by reducing the neutrophil number in the inflammatory site. We investigated the anti-inflammatory activity of QFAE on lipopolysaccharide (LPS)-induced acute lung injury (ALI) mice models and RAW 264.7 cells. QFAE had an anti-inflammatory effect on reducing total cells, neutrophils, and macrophages in BALF and attenuated alveolus collapse, neutrophils infiltration, lung W/D ratio, myeloperoxidase (MPO) protein expression and other pulmonary histological changes in lung tissues, as well as hematological changes. Levels of pro-inflammatory cytokines, including TNF, IL-6, IFN-γ, MCP-1, and IL-12p70, were decreased, whereas anti-inflammatory cytokine IL-10 was increased after treatment with QFAE both in vivo and in vitro . In summary, our results suggested that QFAE had apparent anti-inflammatory effects on CuSO 4 ·5H 2 O-induced zebrafish, LPS-induced ALI mice, and RAW 264.7 cells. Furthermore, QFAE may be a therapeutic drug to treat ALI/ARDS and other respiratory inflammations.
研究领域:
药理学
·
免疫学
·
呼吸医学
·
炎症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2016
·
IF 2.551
Zhilin Qi,Shimei Qi,Liefeng Ling,Jun Lv,Zunyong Feng
Salidroside (SAL) is an active ingredient isolated from the Rhodiola rosea , has potent anti-inflammatory effect, but the mechanism is still elusive. The purpose of this study is to verify the effects of SAL on LPS-induced inflammatory response and investigate the possible underlying molecular mechanism. RAW264.7 cells were pre-incubated with SAL for 2 h, then stimulated with or without LPS for another 16 h. The levels of TNF-α, MCP-1, IL-6, and PGE2 were detected by ELISA , and the production of NO was determined by nitrite analysis. The expression levels of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were detected by Western blotting . In RAW264.7 cells and murine peritoneal macrophages, the activation of signal molecules was also measured by Western blot. The nuclear translocation of STAT3 was determined by Laser confocal and nucleocytoplasmic separation experiments. Our results showed that SAL attenuated the productions of TNF-α, IL-6, MCP-1, PGE2 and NO dose dependently. SAL also suppressed LPS-induced expressions of iNOS and COX-2 significantly. Further studies revealed that SAL down-regulated the phosphorylation of JAK2-STAT3 signaling pathway and reduced the nuclear translocation of STAT3 induced by LPS in RAW264.7 cells and primary peritoneal macrophages. In addition, consistent with the results in vitro, in the model of mice acute lung injury (ALI) induced by LPS, SAL reduced the infiltration of inflammatory cells and decreased the levels of serum TNF-α and IL-6 obviously. Taken together, these data indicated that SAL exerted anti-inflammatory action via down-regulating LPS-induced activation of JAK2-STAT3 pathway and suppressing STAT3 transfer into the nucleus at least in part.
研究领域:
药理学
·
免疫学
·
细胞生物学
·
炎症
✓ 已验证
产品关联
DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2024
·
IF 5.4
Xiaodan Su,Huashuai Zhong,Yongzhu Zeng,Yuyan Zhang,Bo Zhang,Wei Guo,Qiujie Huang,Yong Ye
Background Liver fibrosis is a common stage of various chronic liver diseases, often developing into liver cirrhosis, and even liver cancer. Activated hepatic stellate cells (aHSCs) have been shown to promote the development of liver fibrosis. Therefore, dual-targeted combination therapy for liver may be an effective strategy for the treatment of liver fibrosis. Purpose In this study, the novel nanostructured lipid carriers (GA&GalNH 2 -DC-NLCs) were prepared for Dehydrocavidine (DC), glycyrrhetinic acid (GA) and galactose-PEG 2000 -NH 2 (GalNH 2 ) were selected as targeted ligand-modified nanostructured lipid carriers (NLCs), which enables dual-targeting to the liver for the treatment of liver fibrosis. Study design To study the targeting effect of GA&GalNH 2 -DC-NLCs on liver and its therapeutic effect on liver fibrosis, we established aHSC-T6 cell model and rat model of liver fibrosis for study. Results GA&GalNH 2 -DC-NLCs promoted drug liver targeting efficiency and apoptosis rate by upregulating the expression of Bax. It showed that compared with no and/or GA-modified NLCs and GalNH 2 -modified NLCs, GA&GalNH 2 -DC-NLCs exhibited less extracellular matrix (ECM) deposition, induced apoptosis of aHSCs, and stronger anti-fibrosis effects in vivo. This may be due the fact that GA or GalNH 2 -modifified NLCs simultaneously block HSCs activation and inhibit the IL-6/STAT3 pathway. Conclusion GA&GalNH 2 -DC-NLCs is thus a potential strategy for liver fibrosis treatment.
研究领域:
药学
·
生物技术
·
药理学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Innate Immunity
·
2021
·
IF 2.68
Di Zhao,Bo Yang,Chen Ye,Shaoyi Zhang,Xiaoqiong Lv,Qiyi Chen
Crohn's disease activates the inflammatory reactions to induce intestinal disorders. Enteral nutrition (EN) could exert general immunomodulatory effects. Cecal ligation and perforation (CLP) surgery was utilized to establish Crohn's disease mice models. Survival analysis, hematoxylin-eosin staining, flow cytometry, ELISA, Western blot and liquid chromatography-tandem MS were applied. Baicalein was added to inhibit lipoxygenases. The survival rate was restored and inflammatory injury, exudate neutrophils in peritoneal lavage and serum levels of IL-6 and TNF-α were ameliorated by EN treatment as compared with CLP treatment. EN also increased ILC-3 content, 5/15-LOX level and RvD1-RvD5 in peritoneal lavage. Baicalein reversed all the detected effects of EN except ILC-3 content. EN could activate special pro-resolving mediators (SPMs) through ILCs to mitigate injuries of Crohn's disease.
研究领域:
胃肠病学
·
免疫学
·
营养学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2021
·
IF 6.291
Zekun Li,Jun Guo,Kun Jia,Zhiguo Zheng,Xiaomei Chen,Zhonghui Bai,Yuhao Yang,Bo Chen,Wei Yuan,Weihua Chen,Jian Yang
Oxyfluorfen (OXY) is widely used in agriculture as a herbicide, resulting in its continuous accumulation in the environment. The presence of OXY can be detected in soil and rivers. However, until now, the potential toxicity of OXY to aquatic organisms has not been evaluated. In this study, zebrafish was used as a model animal to evaluate OXY-induced liver toxicity. The study found that 0.25, 0.5, and 1 mg/L of OXY affected the early development of zebrafish and severely damaged the lipid and sugar metabolism in the liver of zebrafish larvae. Furthermore, a metabolic function disorder caused liver damage. OXY also caused inflammation by upregulating the inflammatory factors IL-6 , IL-8 , and TNF-α , and activated the apoptotic pathway to inhibit hepatocyte proliferation, resulting in zebrafish liver toxicity. Our research showed that OXY had certain toxic effects on zebrafish development and liver and could cause potential harm to other aquatic organisms and humans.
研究领域:
环境毒理学
·
水生生物学
·
药理学
✓ 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）