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早田树皮对酸性乙醇诱导的小鼠胃溃疡的胃保护作用。

Gastroprotective effects of Hayata bark against acidic ethanol-induced gastric ulcer in mice.

作者信息

Huang Shih-Cheng, Wu Wen-Jun, Lee Yi-Ju, Tsai Ming-Shiun, Yan Xiang-Zhe, Lin Hsiao-Chun, Lai Pin-Yen, Wang Kun-Teng, Liao Jiunn-Wang, Tsai Jen-Chieh, Wang Sue-Hong

机构信息

Institute of Medicine, Chung Shan Medical University, No. 110, Sec.1, Jianguo N. Road, Taichung, 40201, Taiwan.

Department of Microbiology and Immunology, School of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Road, Taichung, 40201, Taiwan.

出版信息

J Tradit Complement Med. 2023 May 31;13(5):511-520. doi: 10.1016/j.jtcme.2023.05.006. eCollection 2023 Sep.

DOI:10.1016/j.jtcme.2023.05.006
PMID:37693097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10492164/
Abstract

BACKGROUND AND AIM

In traditional medicine, Hayata bark (MZ) is used in combination with other medicines to treat gastric cancer, gastric ulcer (GU), and liver and cardiovascular diseases. This study aims to evaluate the gastroprotective effects and possible mechanism(s) of MZ powder against acidic ethanol (AE)-induced GU and its toxicity in mice.

EXPERIMENTAL PROCEDURE

The gastroprotective effect of MZ powder was analyzed by orally administering MZ for 14 consecutive days before AE-inducing GU. Ulcer index (UI) and protection percentage were calculated, hematoxylin and eosin staining and periodic acid-Schiff staining were performed, and gastric mucus weights were measured. The antioxidative, anti-inflammatory, and anti-apoptotic mechanisms, and possible signaling pathway(s) were studied.

RESULTS AND CONCLUSION

Pretreatment with MZ (100 and 200 mg/kg) significantly decreased 10 μL/g AE-induced mucosal hemorrhage, edema, inflammation, and UI, resulted in protection percentages of 88.9% and 93.4%, respectively. MZ pretreatment reduced AE-induced oxidative stress by decreasing malondialdehyde level and restoring superoxide dismutase activity. MZ pretreatment demonstrated anti-inflammatory effects by reducing both serum and gastric tumor necrosis factor-α, interleukin (IL)-6, and IL-1β levels. Furthermore, MZ pretreatment exhibited anti-apoptotic effect by decreasing Bcl-2 associated X protein/B-cell lymphoma 2 ratio. The gastroprotective mechanisms of MZ involved inactivations of nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) and mitogen activated protein kinase (MAPK) signaling pathways. Otherwise, 200 mg/kg MZ didn't induce liver or kidney toxicity. In conclusion, MZ protects AE-induced GU through mucus secreting, antioxidative, anti-inflammatory, and anti-apoptotic mechanisms, and inhibitions of NF-κB and MAPK signaling pathways.

摘要

背景与目的

在传统医学中,早田树皮(MZ)与其他药物联合用于治疗胃癌、胃溃疡(GU)以及肝脏和心血管疾病。本研究旨在评估MZ粉末对酸性乙醇(AE)诱导的小鼠胃溃疡的胃保护作用及其可能的机制,以及其毒性。

实验步骤

在诱导AE导致GU之前,连续14天口服给予MZ,分析MZ粉末的胃保护作用。计算溃疡指数(UI)和保护率,进行苏木精-伊红染色和过碘酸-希夫染色,并测量胃黏液重量。研究其抗氧化、抗炎和抗凋亡机制以及可能的信号通路。

结果与结论

用MZ(100和200mg/kg)预处理可显著降低10μL/g AE诱导的黏膜出血、水肿、炎症和UI,保护率分别为88.9%和93.4%。MZ预处理通过降低丙二醛水平和恢复超氧化物歧化酶活性来减轻AE诱导的氧化应激。MZ预处理通过降低血清和胃组织中的肿瘤坏死因子-α、白细胞介素(IL)-6和IL-1β水平表现出抗炎作用。此外,MZ预处理通过降低Bcl-2相关X蛋白/B细胞淋巴瘤2比值表现出抗凋亡作用。MZ的胃保护机制涉及核因子κB(NF-κB)和丝裂原活化蛋白激酶(MAPK)信号通路的失活。此外,200mg/kg MZ未诱导肝脏或肾脏毒性。总之,MZ通过黏液分泌、抗氧化、抗炎和抗凋亡机制以及抑制NF-κB和MAPK信号通路来保护AE诱导的GU。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/e89e8b0633af/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/6c8afb9a0ab4/ga1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/5d441d4d2801/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/b8144bae52e1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/92f9e13b7688/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/30b013c2c455/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/db3157a19448/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/cb15515fec63/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/e89e8b0633af/figs1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/6c8afb9a0ab4/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/ec6af5a5b516/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/5d441d4d2801/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/b8144bae52e1/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/92f9e13b7688/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/30b013c2c455/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/db3157a19448/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/cb15515fec63/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed96/10492164/e89e8b0633af/figs1.jpg

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