Department of Biology, The University of Melbourne, Australia.
Department of Zoology, Wildlife and Fisheries, University of Agriculture, Faisalabad, Pakistan.
Food Chem Toxicol. 2024 Aug;190:114816. doi: 10.1016/j.fct.2024.114816. Epub 2024 Jun 14.
Imidacloprid (IMI) is one of the top-notch insecticides that adversely affects the body organs including the liver. Malvidin (MAL) is a natural flavonoid which exhibits a wide range of pharmacological properties. This research was designed to evaluate the protective ability of MAL to counteract IMI instigated liver toxicity in rats. Thirty-two rats were divided into four groups including control, IMI (5mg/kg), IMI (5mg/kg) + MAL (10mg/kg) and MAL (10mg/kg) alone treated group. The recommended dosages were administrated through oral gavage for 4 weeks. It was revealed that IMI intoxication disrupted the PI3K/AKT and Nrf-2/Keap-1 pathway. Furthermore, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme-oxygenase-1 (OH-1) and glutathione reductase (GSR) were reduced while upregulating reactive oxygen species (ROS) and malondialdehyde (MDA) levels after IMI treatment. Moreover, IMI poisoning increased the levels of ALT (Alanine aminotransferase), AST (Aspartate transaminase), and ALP (Alkaline phosphatase) while reducing the levels of total proteins and albumin in hepatic tissues of rats. Besides, IMI administration escalated the expressions of Bcl-2-associated protein x (Bax) and cysteine-aspartic acid protease-3 (Caspase-3) while downregulating the expressions of B-cell lymphoma 2 (Bcl-2). Similarly, IMI intoxication, increased the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, IMI disrupted the normal architecture of hepatic tissues. However, MAL treatment remarkably protected the liver tissues via regulating abovementioned disruptions.
吡虫啉（IMI）是一种顶尖的杀虫剂，它会对包括肝脏在内的身体器官造成不良影响。矢车菊素（MAL）是一种天然类黄酮，具有广泛的药理特性。本研究旨在评估 MAL 对对抗 IMI 引发的大鼠肝毒性的保护能力。将 32 只大鼠分为四组，包括对照组、IMI（5mg/kg）组、IMI（5mg/kg）+MAL（10mg/kg）组和 MAL（10mg/kg）单独处理组。推荐剂量通过口服灌胃给药，持续 4 周。结果表明，IMI 中毒会破坏 PI3K/AKT 和 Nrf-2/Keap-1 通路。此外，IMI 处理后，CAT、GPx、SOD、血红素加氧酶-1（HO-1）和谷胱甘肽还原酶（GSR）的活性降低，而活性氧（ROS）和丙二醛（MDA）水平升高。此外，IMI 中毒会增加 ALT（丙氨酸氨基转移酶）、AST（天冬氨酸氨基转移酶）和 ALP（碱性磷酸酶）的水平，同时降低大鼠肝组织中的总蛋白和白蛋白水平。此外，IMI 给药会增加 Bcl-2 相关蛋白 x（Bax）和半胱氨酸天冬氨酸蛋白酶-3（Caspase-3）的表达，同时降低 B 细胞淋巴瘤 2（Bcl-2）的表达。同样，IMI 中毒会增加白细胞介素-6（IL-6）、核因子 kappa-B（NF-κB）、白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）和环氧化酶-2（COX-2）的水平。此外，IMI 破坏了肝组织的正常结构。然而，MAL 处理通过调节上述破坏显著保护了肝组织。
