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Archive > Volume 16 Issue 2 > 2024,16(2):263-273. DOI:https://doi.org/10.1016/j.chmed.2023.10.006 Prev Next

Rosa odorata var. gigantea的果實(shí)通過調(diào)節(jié)炎癥、氧化應(yīng)激和細(xì)胞凋亡發(fā)揮對(duì)WIRS 誘導(dǎo)的大鼠胃黏膜損傷的保護(hù)作用

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Protective role of fruits of Rosa odorata var. gigantea against WIRS induced gastric mucosal injury in rats by modulating pathway related to inflammation, oxidative stress and apoptosis

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    摘要:
    目的: Rosa odorata var. gigantea 是一種廣受歡迎的藥用植物。一些研究表明，薔薇果實(shí)的乙醇提取物（FOE）具有胃保護(hù)作用。本研究旨在探討 FOE 對(duì)水浸泡應(yīng)激（WIRS）誘導(dǎo)的大鼠胃黏膜損傷的胃保護(hù)活性，并闡明其中可能涉及的分子機(jī)制。 方法: 本研究利用 WIRS 建立了大鼠應(yīng)激性潰瘍模型。大鼠口服FOE的7天后，通過蘇木精和伊紅（H&E）染色分析FOE的治療效果，并通過ELISA實(shí)驗(yàn)檢測(cè)大鼠血液和胃組織中炎癥因子、氧化應(yīng)激因子、胃特異性調(diào)節(jié)因子和胃蛋白酶的變化。免疫組化和 Western blot實(shí)驗(yàn)研究了 FOE 的作用機(jī)制。 結(jié)果: 與 WIRS 組相比，F(xiàn)OE可減輕胃黏膜的宏觀和微觀病理形態(tài)。FOE 能明顯保護(hù)抗氧化劑谷胱甘肽過氧化物酶（GSH-PX）、超氧化物歧化酶（SOD）和過氧化氫酶（CAT）的含量； 抗炎細(xì)胞因子白細(xì)胞介素-10（IL-10）和前列腺素 E2（PGE2）的含量，以及調(diào)節(jié)因子腫瘤壞死因子-α（TGF-α）和體生長(zhǎng)抑素（SS）的含量、 同時(shí)降低丙二醛（MDA）、一氧化氮合酶（iNOS）、腫瘤壞死因子（TNF-α）、白細(xì)胞介素-1β（IL-1β）、白細(xì)胞介素-6（IL-6）、胃泌素（GAS）和內(nèi)皮素（ET）的水平。此外，F(xiàn)OE還明顯上調(diào)了 Nrf2、HO-1、Bcl2 和增殖細(xì)胞核抗原（PCNA）的表達(dá)。此外，F(xiàn)OE 還能激活 p-EGFR 的表達(dá)，下調(diào) NF-κB、Bax、Cleaved-caspase-3、Cyto-C 和 Cleaved-PARP1 的表達(dá)，從而促進(jìn)胃黏膜細(xì)胞的存活。 結(jié)論: 目前的研究表明，F(xiàn)OE對(duì)WIRS引起的胃黏膜損傷具有胃保護(hù)活性。其潛在機(jī)制可能與抗炎、抗氧化和抗細(xì)胞凋亡系統(tǒng)的改善有關(guān)。

    Abstract:
    Objective: Rosa odorata var. gigantea is a popular medicinal plant. Some studies have demonstrated that ethanolic extract of the fruits of R. odorata var. gigantea (FOE) has gastroprotective properties. The aim of this study was to investigate the gastroprotective activity of FOE on water immersion restrained stress (WIRS)-induced gastric mucosal injury in a rat model and elucidate the possible molecular mechanisms involved. Methods: A rat stress ulcer model was established in this study using WIRS. After rats were treated with FOE orally for 7 d, the effect of FOE treatment was analyzed by hematoxylin and eosin (H&E) staining, and the changes of inflammatory factors, oxidative stress factors, and gastric-specific regulatory factors and pepsin in the blood and gastric tissues of rats were examined by ELISA assay. Molecular mechanism of FOE was investigated by immunohistochemical assay and Western blot. Results: Compared with the WIRS group, FOE could diminish both the macroscopic and microscopic pathological morphology of gastric mucosa. FOE significantly preserved the antioxidants glutathione peroxidase (GSH-PX), superoxide dismutase (SOD) and catalase (CAT) contents; anti-inflammatory cytokines interleukin-10 (IL-10) and prostaglandin E2 (PGE2) levels as well as regulatory factors tumor necrosis factor-α (TGF-α) and somatostatin (SS) contents, while decreasing malondialdehyde (MDA), nitric oxide synthase (iNOS), tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), gastrin (GAS) and endothelin (ET) levels. Moreover, FOE distinctly upregulated the expression of Nrf2, HO-1, Bcl2 and proliferating cell nuclear antigen (PCNA). In addition, FOE activated the expression of p-EGFR and downregulated the expression of NF-jB, Bax, Cleaved-caspase-3, Cyto-C and Cleaved-PARP1, thus promoting gastric mucosal cell survival. Conclusion: The current work demonstrated that FOE exerted a gastroprotective activity against gastric mucosal injury induced by WIRS. The underlying mechanism might be associated with the improvement of anti-inflammatory, anti-oxidation and anti-apoptosis systems.

    關(guān)鍵詞:
    抗細(xì)胞凋亡;抗炎;抗氧化;胃黏膜損傷;Rosa odorata Sweet var. gigantea (Coll. et Hemsl.) Rehd. et Wils;水浸束縛型應(yīng)激

    Keywords:


    Project Supported:
    The work was supported by the National Natural Science Foundation of China (No. 81673693) and the National Key R&D Program of China (No. 2017YFD0201402) for financial support.

    Clc Number:

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