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鞣花酸减轻硫酸铍诱导的大鼠脾脏氧化应激和组织病理学改变。

Ellagic acid attenuates beryllium sulphate-induced oxidative stress and histopathological alterations of spleen in rats.

作者信息

Lei Yuandi, Jiang Tianyi, He Liqin, Liu Yanping, Sun Zhanbing, Deng Weihua, Huang Lian, Zhang Zhaohui

机构信息

Department of Preventive Medicine, School of Public Health, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

出版信息

Pharm Biol. 2022 Dec;60(1):1047-1054. doi: 10.1080/13880209.2022.2074051.

Abstract

CONTEXT

Ellagic acid (EA) is a phenolic constituent in certain fruits and has largely been recognized for its role as an antioxidant compound.

OBJECTIVE

To evaluate the effect of EA on beryllium sulphate-induced splenic toxicity in rats.

MATERIALS AND METHODS

Male Sprague-Dawley rats were divided into four groups. The first group was used as control. Group 2 was exposed to BeSO (12 mg/kg, b.w.). Groups 3 and 4 were treated with EA (100 and 300 mg/kg, b.w.) daily for 6 weeks after exposing to BeSO (12 mg/kg, b.w.). Various biochemical and molecular biomarkers were assessed in blood and spleen.

RESULTS

BeSO-intoxicated rats showed significant higher WBC (6.74 ± 0.20 × 10/L vs. 11.02 ± 1.31 × 10/L,  < 0.05), Neu (1.14 ± 0.11 × 10/L vs. 2.45 ± 0.42 × 10/L,  < 0.05), Lym (3.80 ± 0.83 × 10/L vs. 9.64 ± 1.99 × 10/L,  < 0.05), and PLT (868.4 ± 43.2 × 10/L vs. 1408 ± 77.57 × 10/L,  < 0.05) than normal control animals. Moreover, an increase in MDA with depletion of GSH and SOD activity (all  < 0.05) occurred in the spleen of rats treated with BeSO. Furthermore, BeSO-treated rats displayed significantly higher levels of apoptotic markers (Bax, Caspase-3, PARP) (all  < 0.05). EA administration resulted in a significant reversal of hematological and apoptotic markers in beryllium sulphate-intoxicated rats.

DISCUSSION AND CONCLUSIONS

Our results suggest EA treatment exerts a significant protective effect on BeSO-induced splenic toxicity in rats.

摘要

背景

鞣花酸(EA)是某些水果中的一种酚类成分,在很大程度上因其作为抗氧化化合物的作用而被认可。

目的

评估EA对硫酸铍诱导的大鼠脾脏毒性的影响。

材料与方法

将雄性Sprague-Dawley大鼠分为四组。第一组作为对照组。第二组暴露于硫酸铍(12mg/kg,体重)。第三组和第四组在暴露于硫酸铍(12mg/kg,体重)后,每天用EA(100和300mg/kg,体重)处理6周。对血液和脾脏中的各种生化和分子生物标志物进行评估。

结果

硫酸铍中毒的大鼠白细胞(6.74±0.20×10⁹/L对11.02±1.31×10⁹/L,P<0.05)、中性粒细胞(1.14±0.11×10⁹/L对2.45±0.42×10⁹/L,P<0.05)、淋巴细胞(3.80±0.83×10⁹/L对9.64±1.99×10⁹/L,P<0.05)和血小板(868.4±43.2×10⁹/L对1408±77.57×10⁹/L,P<0.05)显著高于正常对照动物。此外,硫酸铍处理的大鼠脾脏中丙二醛增加,谷胱甘肽和超氧化物歧化酶活性降低(均P<0.05)。此外,硫酸铍处理的大鼠凋亡标志物(Bax、Caspase-3、PARP)水平显著升高(均P<0.05)。给予EA可使硫酸铍中毒大鼠的血液学和凋亡标志物显著逆转。

讨论与结论

我们的结果表明,EA处理对硫酸铍诱导的大鼠脾脏毒性具有显著的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e94/9176415/c55192d06d75/IPHB_A_2074051_F0001_B.jpg

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