Arsenic is a potent and toxic heavy metal found in the environment that causes health problems, including liver disease, in humans and animals. Chlorogenic acid (CA) is the most abundant caffeoylquinic acid isomer present in plants. This study aims to assess how CA protects the liver tissue following sodium arsenite (NaAsO2)-induced toxicity in mice. Male Swiss mice were allocated into 5 groups: Control, intragastrically administered CA (200 mg/kg), intragastrically administered NaAsO2 (5 mg/kg), and two groups administered with CA (100 and 200 mg/kg) and NaAsO2. CA was administered 30 min before NaAsO2 and all the mice were treated daily for 28 days. To investigate the biochemical, histopathological, immunohistochemical, and molecular changes, blood and liver samples were collected. NaAsO2 treatment increased the liver function biomarkers such as alanine transaminase, aspartate transaminase, alkaline phosphatase, and total bilirubin. Lipid and nitric oxide production was elevated. Glutathione content and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase decreased, indicating a disturbance in redox homeostasis. Histopathological examination revealed a granular degeneration of hepatocytes, infiltration of inflammatory cells, and centrilobular hepatocyte necrosis. Furthermore, tumor necrosis factor-α and interleukin-1β were upregulated upon NaAsO2 treatment, suggesting the induction of inflammation. Moreover, NaAsO2 triggered apoptosis in the liver by upregulating Bax and caspase-3 and downregulating Bcl-2. However, CA abrogated the biochemical, molecular, and histological changes, reflecting its hepatoprotective role in response to NaAsO2 treatment. Our findings demonstrate that CA could be a potential therapeutic to minimize NaAsO2-induced hepatic injury.

中文翻译：

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绿原酸可预防砷治疗小鼠的肝毒性：氧化应激和细胞凋亡的作用。

砷是在环境中发现的有力和有毒的重金属，会导致人类和动物的健康问题，包括肝脏疾病。绿原酸（CA）是植物中存在的最丰富的咖啡酰奎尼酸异构体。这项研究旨在评估CA如何保护砷化钠（NaAsO2）诱导的小鼠毒性后的肝脏组织。将雄性Swiss小鼠分为5组：对照组，胃内给予CA（200 mg / kg），胃内给予NaAsO2（5 mg / kg）和两组分别给予CA（100和200 mg / kg）和NaAsO2。在NaAsO2之前30分钟施用CA，每天对所有小鼠进行28天的治疗。为了研究生物化学，组织病理学，免疫组织化学和分子变化，收集了血液和肝脏样品。NaAsO2处理可增加肝功能生物标志物，如丙氨酸转氨酶，天冬氨酸转氨酶，碱性磷酸酶和总胆红素。脂质和一氧化氮的产生增加。谷胱甘肽含量和超氧化物歧化酶，过氧化氢酶，谷胱甘肽过氧化物酶和谷胱甘肽还原酶的活性下降，表明氧化还原稳态受到干扰。组织病理学检查显示肝细胞出现颗粒状变性，炎性细胞浸润和小叶肝细胞坏死。此外，在NaAsO 2处理中，肿瘤坏死因子-α和白介素-1β被上调，提示炎症的诱导。此外，NaAsO2通过上调Bax和caspase-3并下调Bcl-2来触发肝细胞凋亡。但是，CA废除了生化，分子，和组织学变化，反映了其对NaAsO2处理的保肝作用。我们的发现表明，CA可能是将NaAsO2引起的肝损伤降至最低的潜在疗法。