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新型席夫碱CdCl2(C14H21N3O2)化合物通过Bax/HSP-70信号通路和炎性细胞因子产生的体内胃保护作用

In Vivo Gastroprotective Upshots of the Novel Schiff Base CdCl2 (C14H21N3O2) Compound by Bax/HSP-70 Signaling and Inflammatory Cytokines.

作者信息

Shareef Suhayla H

机构信息

Department of Biology, College of Education, Salahaddin University-Erbil, Erbil, IRQ.

出版信息

Cureus. 2024 Dec 18;16(12):e75963. doi: 10.7759/cureus.75963. eCollection 2024 Dec.

DOI:10.7759/cureus.75963
PMID:39830532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11741513/
Abstract

BACKGROUND

Synthesis of the original Schiff base CdCl (CHNO) compound (Schiff base complex) displays an extensive range of bioactivities and was predictably utilized to treat several syndromes.

PURPOSE

The goal of the existing experiment is to evaluate the gastroprotective effects of a novel Schiff base CdCl₂ (C14H21N3O2) compound in alcohol-induced gastric ulcers in rats by examining its antioxidant activity, anti-inflammatory effects, and modulation of key molecular markers, including heat shock protein-70 (HSP-70) and Bcl-2-associated X protein (Bax) proteins.

METHODS

Five groups of rats were utilized in the current study. Control and model groups were orally administered 10% Tween 20. The treated groups were orally administered 20 mg/kg omeprazole or Schiff base compound (25 or 50 mg/kg). One hour later, only the control group received oral 10% Tween 20, and the treated groups received oral (5 ml/cage) absolute alcohol. During the second hour, all rats were sacrificed.

RESULTS

All treated rats presented considerable improvement in alcohol-induced gastric injury recognized by decreasing ulcer index and raising % of ulcer inhibition. Increased mucus and gastric pH content and decreased ulcerated portion, reduced or non-appearance of edema, and leucocytes penetrated the subcutaneous layer. In stomach epithelium homogenate, the Schiff base compound obtainable significant upsurge superoxide dismutase (SOD), catalase (CAT) activities, considerable declining malondialdehyde (MDA) quantity. Moreover, the Schiff base compound raised the intensity of periodic acid-Schiff (PAS) stains gastric epithelium. Furthermore, the Schiff base compound formed up-regulated HSP-70 and down-regulated Bax proteins gastric epithelium Schiff base compound, reduced the level of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and improved the quantity of IL-10. Administering a high dose of 500 mg/kg Schiff base compound revealed the nontoxic nature of the compound in rats.

CONCLUSION

Schiff base compound exhibited gastroprotective effects attributed to its antioxidant nature, its capability to enhance mucus excretion, SOD and CAT, reduce MDA amount, up-regulate HSP-70 protein, down-regulate Bax protein, and inflammatory cytokines.

摘要

背景

原始席夫碱CdCl (CHNO) 化合物(席夫碱配合物)的合成显示出广泛的生物活性,并且可预见地被用于治疗多种综合征。

目的

现有实验的目的是通过检测一种新型席夫碱CdCl₂ (C14H21N3O2) 化合物的抗氧化活性、抗炎作用以及对关键分子标志物(包括热休克蛋白-70 (HSP-70) 和Bcl-2相关X蛋白 (Bax))的调节作用,来评估其对大鼠酒精性胃溃疡的胃保护作用。

方法

本研究使用了五组大鼠。对照组和模型组口服10%吐温20。治疗组口服20 mg/kg奥美拉唑或席夫碱化合物(25或50 mg/kg)。一小时后,仅对照组口服10%吐温20,治疗组口服(5 ml/笼)无水乙醇。在第二个小时期间,所有大鼠均被处死。

结果

所有治疗组大鼠在酒精性胃损伤方面均有显著改善,表现为溃疡指数降低和溃疡抑制率提高。黏液和胃pH值含量增加,溃疡部分减少,水肿减轻或消失,白细胞未穿透皮下层。在胃上皮匀浆中,席夫碱化合物可使超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 活性显著升高,丙二醛 (MDA) 含量显著降低。此外,席夫碱化合物提高了胃上皮过碘酸-希夫 (PAS) 染色的强度。此外,席夫碱化合物使胃上皮中HSP-70蛋白上调,Bax蛋白下调,降低了肿瘤坏死因子-α (TNF-α)、白细胞介素-6 (IL-6) 的水平,并提高了IL-10的量。给予500 mg/kg高剂量的席夫碱化合物显示该化合物在大鼠中无毒。

结论

席夫碱化合物表现出胃保护作用,这归因于其抗氧化性质、增强黏液分泌的能力、提高SOD和CAT水平、降低MDA含量、上调HSP-70蛋白、下调Bax蛋白以及调节炎性细胞因子的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/25d24ee7359c/cureus-0016-00000075963-i09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/65abc09d5682/cureus-0016-00000075963-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/7420ddbbf4e3/cureus-0016-00000075963-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/01519ea0306e/cureus-0016-00000075963-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/e88be1e6fdb5/cureus-0016-00000075963-i04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/8c4130810ff4/cureus-0016-00000075963-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/e7b80824ec22/cureus-0016-00000075963-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/49feefef9988/cureus-0016-00000075963-i07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/90f8d22cca46/cureus-0016-00000075963-i08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/25d24ee7359c/cureus-0016-00000075963-i09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/65abc09d5682/cureus-0016-00000075963-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/7420ddbbf4e3/cureus-0016-00000075963-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/01519ea0306e/cureus-0016-00000075963-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/e88be1e6fdb5/cureus-0016-00000075963-i04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/8c4130810ff4/cureus-0016-00000075963-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/e7b80824ec22/cureus-0016-00000075963-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/49feefef9988/cureus-0016-00000075963-i07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/90f8d22cca46/cureus-0016-00000075963-i08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9c4b/11741513/25d24ee7359c/cureus-0016-00000075963-i09.jpg

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