JOURNAL OF ETHNOPHARMACOLOGY
·
2024
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IF 4.8
Jiaying Liu,Yuanfan Chen,Jing Zhang,Yun Zheng,Yun An,Chenglai Xia,Yonger Chen,Song Huang,Shaozhen Hou,Dong Deng
Ethnopharmacological relevance The dried fruit of Crataegus pinnatifida Bunge (Hawthorn in Chinese) is a traditional medicine used in China, Japan and Korea for thousands of years. Hawthorn is documented in the Chinese Pharmacopoeia , as a folk medicine that is used to eliminate food, strengthen the stomach, move qi and dissipate blood stasis, treat stagnation of meat and food, gastric distention and fullness, and has anti-inflammatory effects. Vitexin, a flavonoid glycoside, is an important biologically active compound derived from Hawthorn, with significant antioxidant and anti-inflammatory properties. The pharmacological effects of Hawthorn are highly correlated with the antioxidant and anti-inflammatory effects of vitexin. Aim of the study The aim of the present study was to investigate the effect of vitexin on the alleviation of chronic atrophic gastritis (CAG) induced by 1-methyl-3-nitro-1-nitrosoguanidine (MNNG) in a rat model, as well as to elucidate the underlying mechanisms involved. Materials and methods CAG was administered at a concentration of 170 μg/mL MNNG in the drinking water of rats, and the effects of vitexin (30 mg/kg, once daily for 6 weeks) on gastric tissues were subsequently analyzed. Pathological damage was assessed using H&E and AB-PAS staining. Gastrointestinal hormone levels, specifically motilin (MTL) and gastrin (GAS), were quantified using biochemical index determination kits. To evaluate the levels of cytokines, specifically IL-1β and IL-18, in gastric tissue, an enzyme-linked immunosorbent assay (ELISA) was performed. Additionally, to investigate the effects of vitexin on the NLRP3 inflammasome, GES-1 cells were subjected to treatment with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). The targeting of NLRP3 by vitexin was assessed in vitro using CESTA, DARTS, and a synthesized biotin-labeled vitexin probe (biotin-vitexin) in conjunction with dual immunofluorescence. RT-PCR, Western blotting and immunofluorescence were used to evaluate the ameliorative effect of oysterin on LPS + ATP-induced GES-1 cells in vitro. Results Administration of vitexin significantly alleviated the symptoms of chronic atrophic gastritis (CAG) by reducing weight loss and minimizing gastric tissue damage. Treatment with vitexin in CAG rats effectively reduces the production of pro-inflammatory cytokines. Furthermore, vitexin attenuated the activation of the NLRP3 inflammasome in CAG induced by MNNG. Mechanistic experiments showed that NLRP3 is a direct cellular target of vitexin, while vitexin inhibited rat NLRP3 inflammasome. Conclusion Vitexin mitigates MNNG-induced CAG, and its protective effect is linked to the inhibition of NLRP3 inflammasome activation.
研究领域:
药理学
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民族药理学
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胃肠病学
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产品关联
DOI
PubMed
高影响因子
CELL BIOCHEMISTRY AND BIOPHYSICS
·
2024
·
IF 1.8
Jiang Qianqian,Fan Guoxia,Wu Kaiwei
Chronic atrophic gastritis (CAG) is a critical initial step in gastric cancer tumorigenesis accompanied by high malignancy. Erianin has been proposed as a promising agent in treating precancerous lesions of gastric cancer. Considering that little work has been implemented concerning the specific role and possible regulatory mechanism of Erianin in CAG, the goal of the study is to disclose the effects and mechanism of erianin on the malignant transformation in the process of CAG. CAG cell model was generated in human gastric epithelium GES-1 cells induced by Nmethyl-N’-nitro-N-nitrosoguanidine (MNNG). CCK-8 method determined cell viability. ELISA and corresponding assay kits severally appraised the contents of inflammatory cytokines and oxidative stress markers. Cellular reactive oxygen species (ROS) formation was measured by flow cytometry analysis using DCFH-DA probe. GFP-LC3 immunofluorescence staining and Western blotting evaluated autophagy. Also, Western blotting analyzed the expression of components in mitogen activated protein kinase (MAPK)/mechanistic target of rapamycin (mTOR) signaling. The results manifested that MNNG treatment diminished the viability and autophagy whereas intensified the inflammation and oxidative stress in GES-1 cells, which were all reversed by Erianin. Besides, Erianin blocked mTOR/MAPK signaling in MNNG-exposed GES-1 cells. Autophagy inhibitor 3-methyladenine (3-MA) or p38 MAPK agonist asiatic acid partially counteracted the protection elicited by Erianin against viability loss, inflammatory reaction as well as oxidative stress in MNNG-induced GES-1 cells. Combined with the findings, Erianin might mediate autophagy to improve MNNG-elicited CAG via MAPK/mTOR signaling.
研究领域:
肿瘤学
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胃肠病学
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药理学
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细胞生物学
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DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2021
·
IF 5.811
Tong Yuling,Liu Liping,Wang Ruilin,Yang Tao,Wen Jianxia,Wei Shizhang,Jing Manyi,Zou Wenjun,Zhao Yanling
The purpose of this study was to investigate the therapeutic effect of berberine (BBR) on MNNG-induced chronic atrophic gastritis (CAG) and the possible mechanism of BBR through TGF-β1/PI3K signal pathway. GES-1 were pretreated with MNNG for 2 h before BBR treatment in all procedures. Cell viability was quantified by cell counting kit-8, and GES-1 morphology and proliferation were detected by high content screening (HCS) assay. The rat model of CAG was established by MNNG, and the therapeutic effect of BBR on stomach histopathology and serum supernatant were analyzed in vivo. In addition, the possible mechanism of BBR was further discussed, and the expression of related genes and proteins in TGF-β1/PI3K signal pathway was detected. The results showed that BBR could significantly improve the survival rate and morphological changes of GES-1, improve the gastric tissue injury of CAG rats, and reduce the expression of G-17 and inflammatory factors IL-8, TNF-α, IL-6 and IL-1β. In addition, BBR down-regulated the expression of TGF-β1 axis-related signals such as TGF-β1, PI3K, p-Akt/Akt, p-mTOR/mTOR and P70S6K, and promoted the expression of PTEN, LC3-II and Beclin-1. In Conclusion, BBR can improve CAG which may be closely related to TGF-β1/PI3K signal pathway.
研究领域:
药理学
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胃肠病学
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2024
·
IF 4.8
Suizhi Cheng,Jin Chen,Qianhui Li,Yuhong Nie,Ting Ni,Caiting Peng,Xi Luo,Yasin Pazilat,Shumin Zhang,Jiancai Tang,Zhenzhong Liu
Recent research has revealed that N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) constitutes a significant risk factor in the development of esophageal cancer. Several investigations have elucidated the beneficial impact of folic acid (FA) in safeguarding esophageal epithelial cells against MNNG-induced damage. Therefore, we hypothesized that FA might prevent MNNG-induced proliferation of esophageal epithelial cells by interfering with the PI3K/AKT/mTOR signaling pathway. In vivo experiments, we found that FA antagonized MNNG-induced proliferation of rat esophageal mucosal epithelial echinocytes and activation of the PI3K/AKT/mTOR signaling pathway. In our in vitro experiments, it was observed that acute exposure to MNNG for 24 h led to a decrease in proliferative capacity and inhibition of the PI3K/AKT/mTOR signaling pathway in an immortalized human normal esophageal epithelial cell line (Het-1A), which was also ameliorated by supplementation with FA. We successfully established a Het-1A-T-cell line by inducing malignant transformation in Het-1A cells through exposure to MNNG. Notably, the PI3K/AKT2/mTOR pathway showed early suppression followed by activation during this transition. Next, we observed that FA inhibited cell proliferation and activation of the PI3K/AKT2/mTOR signaling pathway in Het-1A-T malignantly transformed cells. We further investigated the impact of 740Y-P, a PI3K agonist, and LY294002, a PI3K inhibitor, on Het-1A-T-cell proliferation. Overall, our findings show that FA supplementation may be beneficial in safeguarding normal esophageal epithelial cell proliferation and avoiding the development of esophageal cancer by decreasing the activation of the MNNG-induced PI3K/AKT2/mTOR signaling pathway.
研究领域:
肿瘤学
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细胞生物学
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分子生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2021
·
IF 4.36
Yuling Tong,Ruilin Wang,Xia Liu,Miao Tian,Yanling Wang,Yanfei Cui,Wenjun Zou,Yanling Zhao
Ethnopharmacological relevance Zuojin Pill (ZJP) is a classic prescription composed of Coptis chinensis and Tetradium ruticarpum (A.Juss.) T.G.Hartley, which is often used in the treatment of digestive system diseases . Aim of this study The purpose of this study was to explore the therapeutic effect and potential mechanism of ZJP on chronic atrophic gastritis (CAG) induced by MNNG . Materials and methods The GES-1 and rat model of CAG was established by MNNG. Detection of cell viability, morphological changes and proliferation of GES-1 by CCK-8 and high content screening (HCS) assay. G-17, IL-8 and TNF-α in rat serum were detected by ELISA kit. The expression of related mRNA and protein on TGF-β1/PI3K/Akt signal axis were detected by RT-PCR and Western blot . Results The results showed that ZJP could significantly improve the GES-1 damage induced by MNNG and improve the gastric histomorphology of CAG rats. The intervention of ZJP could significantly reduce the content of G-17 and inflammatory factors IL-8, TNF- α, IL-6 and IL-1β, inhibit the expression of TGF-β1, PI3K and their downstream signals p-Akt, p-mTOR, P70S6K, and promote the expression level of PTEN, LC3-II and Beclin-1. Conclusion ZJP has a good therapeutic effect on CAG induced by MNNG, which may be closely related to the inhibition of TGF-β1/PI3K/Akt signal pathway.
研究领域:
药理学
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民族药理学
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胃肠病学
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF HAZARDOUS MATERIALS
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2024
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IF 12.2
Qing Wang,Yefei Huang,Min Jiang,Yu Tang,Qinzhi Wang,Longlong Bai,Chenglong Yu,Xinyue Yang,Kun Ding,Weimin Wang,Jin Bai,Yansu Chen
N-Nitroso compounds (NOCs) are recognized as important factors that promote gastric cancer development, but the specific effects and potential mechanisms by which NOC exposure promotes gastric cancer are still poorly understood. In this study, we explored the effects and potential molecular mechanisms of NOCs on the promotion of gastric cancer using methylnitronitrosoguanidine (MNNG), a classical direct carcinogen of NOC. The results of in vivo and in vitro experiments showed that chronic and low-concentration MNNG exposure significantly promoted the malignant progression of tumors, including cell migration, cell invasion, vasculogenic mimicry (VM) formation, cell spheroid formation, stem cell-like marker expression, and gastric cancer growth and metastasis. Mechanistically, we revealed that demethylase ALKBH5 regulated the level of the N6‑methyladenosine (m6A) modification in the 3′UTR and CDS region of the ZKSCAN3 mRNA to promote ZKSCAN3 expression, mediated the binding of ZKSCAN3 to the VEGFA promoter region to regulate VEGFA transcription, and participated in MNNG-induced gastric cancer cell migration, invasion, VM formation, cell spheroid formation, stem cell-like marker expression and ultimately gastric cancer progression. In addition, our study revealed that ALKBH5-ZKSCAN3-VEGFA signaling was significantly activated during MNNG-induced gastric carcinogenesis, and further studies in gastric cancer patients showed that ALKBH5, ZKSCAN3, and VEGFA expression were upregulated in cancers compared with paired gastric mucosal tissues, that ALKBH5, ZKSCAN3, and VEGFA could serve as important biomarkers for determining patient prognosis, and that the molecular combination showed greater prognostic value. These findings provide a theoretical basis for developing gastric cancer interventions for NOCs and for determining gastric cancer progression.
研究领域:
肿瘤学
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分子生物学
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癌症生物学
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表观遗传学
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产品关联
DOI
PubMed
高影响因子
COMBINATORIAL CHEMISTRY & HIGH THROUGHPUT SCREENING
·
2025
·Vol. 29
·期 4
·717-730
·
IF 1.7
Yuling Wei,Wenhui Wu,Min Duan,Ting Li,Mei Liu,Jinyan Li
IntroductionChronic atrophic gastritis (CAG) is the initial phase in the carcinogenesis of gastric cancer (GC). Therefore, effective treatment for CAG is important in reducing the risk of GC progression. As an isoflavone compound, formononetin (FMN) has been identified as a potential therapeutic agent for acute gastric ulcers and GC. However, no study has reported the protective effect of FMN against CAG and its underlying mechanism. This study aimed to explore the therapeutic effects of FMN on CAG and its underlying mechanisms in vitro.MethodsNetwork pharmacology was applied to predict the core targets of FMN therapy in CAG. The CAG cell model was developed using N-methyl-N’-nitro-N-nitrosoguanidine (MNNG)-triggered human gastric epithelial cells (GES-1). The CCK-8 assay was applied to estimate cellular viability. The expression of inflammatory cytokines in cell supernatant was detected by ELISA. The protein levels and localization of nuclear receptor coactivator 1 (NCOA1), c-Jun, and c-Fos were evaluated using western blotting and immunofluorescence staining. Cell apoptosis was measured using flow cytometry.ResultsNetwork pharmacology analysis identified c-Jun as the core target of FMN in the treatment of CAG, with biological processes primarily involving the regulation of apoptosis and inflammation. In vitro, MNNG exposure reduced GES-1 cell viability as well as increased inflammation and cellular apoptosis, and these effects were reversed by FMN treatment. In detail, FMN decreased the protein levels of NCOA1, c-Jun, and c-Fos in MNNG-triggered GES-1 cells. The activator protein-1 (AP-1) inhibitor T-5224 enhanced the effects of FMN treatment on cell viability, inflammatory response, and apoptosis in MNNG-triggered GES-1 cells.DiscussionThis study employed network pharmacology analysis to identify FMN's therapeutic targets for CAG and validated the underlying mechanisms in vitro. While these results are promising, in vivo validation is required to confirm the efficacy of FMN. A comparative pharmacological evaluation against existing therapeutic agents and bioactive compounds would further elucidate FMN's therapeutic potential for CAG treatment.ConclusionFMN ameliorated the cell damage that MNNG triggered in GES-1 cells. The mechanism involved the anti-inflammatory and anti-apoptotic effects of FMN via modulation of the NCOA1/AP-1 signaling axis. The present preliminary study found FMN to exhibit a potential therapeutic effect against CAG.
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DOI
高影响因子
Evidence-based Complementary and Alternative Medicine
·
2021
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IF 2.63
Yuling Tong,Manyi Jing,Xu Zhao,Honghong Liu,Shizhang Wei,Ruisheng Li,Xia Liu,Min Wang,Hongtao Song,Yanling Zhao
The classic prescription Zuojin Pill (ZJP) shows a good therapeutic effect on chronic atrophic gastritis (CAG); it is of great significance to clarify its specific mechanism. Therefore, we explore the mechanism of ZJP on MNNG-induced CAG by integrating approaches. First of all, through the pathological changes of gastric tissue and the expression level of PGI and PGI/II in serum, the expression of inflammation-related factors was determined by RT-PCR to determine the efficacy. Then, UPLC-Q-TOF/MS was used for plasma and urine metabolomic analysis to screen the specific potential biomarkers and metabolic pathway of ZJP in ameliorating CAG and to explore its possible mechanism. ZJP significantly ameliorate the pathological injury of gastric tissue, increase levels of PGI and PGI/II, and reduce the expression level of proinflammatory factors. Through metabolomic analysis, 9 potential metabolic differences were identified and 6 related metabolic pathways were enriched. These findings indicate for the first time the potential mechanism of ZJP in improving CAG induced by MNNG and are of great significance to the clinical development and application of ZJP-related drugs.
研究领域:
中药学
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代谢组学
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病理学
✓ 已验证
DOI
高影响因子
MOLECULAR AND CELLULAR BIOCHEMISTRY
·
2026
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IF 4.7
Zhang Pan,Sun Xuelin,Liu Longteng,Zhang Yatong,Bo Jiaqi,Huang Wenli,Na Yifan,Zhang Jingyi,Qin Xiaoyun,Luo Qingfeng
Gastric precancerous lesions (GPLs) are a pivotal stage in the gastritis-gastric cancer sequence, and the absence of effective treatments presents a clinical challenge. Veratramine is a natural anti-inflammatory and analgesic steroid alkaloid; however, its effects on GPLs and the mechanisms have remained unexplored. This study investigated the effects of veratramine on GPLs using 1-Methyl-3-nitro-1-nitrosoguanidine (MNNG)-induced GES-1 cells and rat models, utilizing RNA-seq to elucidate the underlying mechanisms. In vitro, veratramine inhibited malignant cells (MC) proliferation, induced apoptosis, and triggered G0/G1 cell cycle arrest. It also suppressed epithelial-mesenchymal transition (EMT), migration, and invasion by upregulating E‑cadherin and downregulating Slug and vimentin. Transcriptomic and molecular docking analyses highlighted the Wnt/β-catenin pathway as a key target, regulated via DDX60, MUC1, APOL1, and MSH5. Veratramine reduced Wnt10B, β-catenin, and cyclin D1 expression and blocked β‑catenin nuclear translocation; these effects were reversed by the Wnt activator BML-284. In vivo, treatment with veratramine ameliorated the GPLs-induced pathological changes in rats. It restored body weight and preserved gastric mucosal integrity, as evidenced by intact glandular and cellular morphology, reduced hyperplasia, and attenuated intestinal metaplasia. These improvements were associated with a modulation of key molecular markers, specifically a decrease in the expression of N-cadherin, Wnt10B, and β-catenin, alongside an increase in E-cadherin expression in gastric tissues. These results collectively indicate that veratramine exerts its therapeutic effects against GPLs primarily by suppressing the Wnt/β-catenin signaling pathway. Taken together, our findings suggest that veratramine is a promising candidate small-molecule drug for the treatment of GPLs.
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2025
·
IF 5.4
Xiao Zhang,Zhekai Huang,Xuejun Hu,Yu Tang,Xiaofeng Zhong,Li Li,Liujing Ni,Fang Li,Haibing Hua,Fangshi Zhu
Ethnopharmacological relevance Wendan Decoction (WDD) is a classical prescription deeply rooted in traditional Chinese medicine (TCM), originally documented by Sun Simiao in Beiji Qianjin Yaofang during the Tang Dynasty. Traditionally, it has been used to treat disorders associated with phlegm-dampness accumulation and digestive dysfunction, reflecting the TCM principle of harmonizing the stomach and resolving dampness. Within the clinical practice at Jiangyin Hospital Affiliated to Nanjing University of Chinese Medicine, WDD is employed for the treatment of chronic atrophic gastritis (CAG), continuing its long-standing application in gastrointestinal disorders. Despite its widespread traditional use and cultural significance, the active constituents and precise pharmacological mechanisms of WDD have not yet been fully elucidated. Purpose This study aimed to systematically investigate the material basis and therapeutic mechanisms of WDD in CAG treatment. Methods The bioactive constituents of WDD were first identified using high-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry (HPLC-Q-TOF-MS/MS). To evaluate its therapeutic effects, we established both in vivo and in vitro models of chronic atrophic gastritis (CAG). For the in vivo studies, a rat CAG model was generated through a multi-factor compound induction approach, whereas in vitro cellular injury was induced using N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). To elucidate the underlying mechanisms, we integrated network pharmacology to predict candidate targets and signaling pathways, followed by experimental verification via immunohistochemical staining and Western blot analysis. Results HPLC-Q-TOF-MS/MS profiling revealed 34 bioactive constituents in WDD, with naringin, neohesperidin, and narirutin identified as key components. In vivo investigations demonstrated that WDD administration markedly improved gastric histopathological alterations in CAG model rats, accompanied by increased serum levels of pepsinogen I (PG I) and pepsinogen II (PG II), along with reduced gastrin-17 (G-17) and interleukin-6 (IL-6) concentrations. In vitro studies further showed that WDD treatment inhibited cell proliferation, migration, and invasive potential in MNNG-transformed MC cells. Network pharmacology-based analysis predicted that the therapeutic efficacy of WDD against CAG was primarily mediated via the JAK/STAT signaling axis. Subsequent mechanistic validation confirmed that WDD significantly attenuated the phosphorylation of JAK2 and STAT3, suggesting its inhibitory effect on the JAK2/STAT3 pathway. Conclusion This study revealed that WDD exerted therapeutic effects on CAG through suppression of the JAK2/STAT3 pathway. Our findings elucidate the pharmacological mechanisms of WDD and provide a scientific basis for its traditional use in managing CAG, highlighting its potential as a therapeutic candidate worthy of further clinical investigation.
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产品关联
DOI
PubMed
高影响因子
TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2022
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IF 4.46
Suizhi Cheng,Li Che,Qingqing Yang,Rongjing Sun,Yuhong Nie,Haoyue Shi,Yiwen Ding,Li Wang,Zuo Du,Zhenzhong Liu
N -methyl- N′ -nitro- N -nitrosoguanidine (MNNG) is a common alkylating agent , which can be experimentally used as a chemical mutagen and carcinogen, extensively existing in the environment. Folic acid (FA), part of the B group of vitamins, plays an important role in defending against inflammation and reducing the risk of cancers. Nevertheless, there is little research on the protective effects of FA against MNNG-induced esophageal inflammation, and its underlying mechanism still remains elusive. Hence, in the present study, we exposed MNNG to SD rats and esophageal cells to establish the esophageal inflammation models. Our research aims to explore the protective roles of FA against esophageal inflammation induced by MNNG via NF-κB pathway by CCK-8, EdU, RT-qPCR, ELISA , H&E, Western blot . Our results revealed that MNNG decreased the viability of esophageal cells, which was restored under FA intervention. Besides, FA relieved the elevation of IL-6, IL-8 and TNF-α in MNNG-induced esophageal inflammation. Moreover, histopathological analysis showed that epithelial spinous cells proliferated in mucous layer, and inflammatory cells were locally infiltrated in the submucosa after MNNG exposure, while the pathological damage of esophageal tissues was gradually alleviated along with increasing FA doses. And Western blot results demonstrated that FA could relieve the rise of phosphorylated IκBα (p-IκBα) and phosphorylated p65 (p-p65) proteins induced by MNNG. Therefore, it is reasonable to believe that FA has a crucial role in preventing MNNG-induced esophageal inflammation through inhibiting the NF-κB pathway, thereby down-regulating the expressions of IL-6, IL-8 and TNF-α.
研究领域:
药理学
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毒理学
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分子生物学
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病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2024
·
IF 4.8
Jia Liu,Mengyu Li,Guobao Chen,Junhui Yang,Ying Jiang,Fang Li,Haibing Hua
Ethnopharmacological relevance Jianwei Xiaoyan Granule (JWXYG) is the traditional Chinese medicine preparation in Jiangyin Hospital Affiliated to Nanjing University of Chinese Medicine, which has been widely used in clinical treatment of chronic atrophic gastritis (CAG). However, the material basis and potential mechanism of JWXYG in the treatment of CAG are not clear. Purpose To explore the material basis and potential mechanism of JWXYG in the treatment of CAG. Methods In this study, the components of JWXYG were analyzed by HPLC-Q-TOF-MS/MS. Then, the CAG model in rats established by a composite modeling method and MC cell model induced by MNNG were used to explore the improvement effect of JWXYG on CAG. Finally, the potential mechanism of JWXYG in the treatment of CAG was preliminarily predicted based on network pharmacology and validated experimentally. Results Thirty-one components of JWXYG were analyzed through HPLC-Q-TOF-MS/MS, such as albiflorin , paeoniflorin , lobetyolin firstly. Research results in vivo showed that the gastric mucosa became thinner, intestinal metaplasia appeared, the number of glands was reduced, the serum levels of PG I and PG II increased and the contents of G17 and IL-6 reduced in CAG model rats. After 4 weeks of JWXYG (2.70 g/kg) administration, these conditions were significantly improved. In addition, cell viability , migration, and invasion of MNNG-induced MC cells was inhibited by JWXYG treatment (800 μg/mL). Furthermore, the results of network pharmacology indicated that HIF-1 and VEGF signaling pathways might play important roles in the therapeutic process. Then the results of Western blot , immunohistochemistry and immunofluorescence confirmed that with JWXYG treatment, the increased expression of HIF-1α, VEGF and VEGFR2 in gastric issue of CAG rats were restrained. Eventually, potential components of JWXYG in the treatment of CAG were predicted through molecular docking to elucidate the material basis. Conclusion JWXYG could inhibit angiogenesis by regulating HIF-1α-VEGF pathway to exert therapeutic effects on CAG. Our study explored the potential mechanisms and material basis of JWXYG in the treatment of CAG and provides experimental data for the clinical rational application of JWXYG.
研究领域:
药理学
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中医中药
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分子生物学
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病理学
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产品关联
DOI
PubMed
高影响因子
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