Paraquat (PQ) is an effective herbicide however, due to its adverse effects on different organs including heart, it is considered as highly toxic to human beings. Kaempferide (KMF) is a plant-based flavonoid with conspicuous pharmacological properties. This experiment was executed to evaluate the palliative actions of KMF on PQ prompted cardiac toxicity in rats. Twenty-four rats were apportioned into 4 equal groups which were designated as control, toxicant (PQ treated), Co-treated (PQ + KMF) and KMF group. After 30 days of treatment, PQ intoxication resulted in a remarkable reduction in antioxidant enzymes activities which include, glutathione reductase (GSH), glutathione S-transferase (GST), catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and glutathione disulfide reductase (GSR), whereas an elevation was observed in reactive oxygen species (ROS), & malondialdehyde (MDA) as well as hydrogen peroxide (H₂O₂) level. Furthermore, concentrations of cardiac injury markers, creatinine phosphokinase (CPK), creatine kinase-myoglobin binding (CK-MB), & lactate dehydrogenase (LDH), as well as troponin I were increased in response to PQ treatment. Moreover, inflammatory cytokines such as tumour necrosis factor alpha (TNF-α), nuclear factor-kappa B (NF-κB), and interleukin-6 (IL-6), interleukin-1 beta (lL-1β), and cyclooxygenase-2 (COX-2) levels were augmented in PQ intoxicated group. PQ exposure reduced the gene expression of cardiac anti-apoptotic markers (Bcl-2), but the gene expression of apoptotic marker (caspase-9, caspase-3 and Bax) was increased. Histopathological damages were also observed in toxicant (PQ) exposed group. However, the administration of KMF significantly palliated PQ induced aforementioned disruptions. In the light of these findings, it is concluded that KMF is a promising bioactive compound that may be used as a curative agent against PQ instigated cardiac damage due to its marvelous antioxidant, anti-apoptotic, anti-inflammatory as well as cardioprotective potential.

百草枯（PQ）是一种有效的除草剂，但由于其对包括心脏在内的不同器官产生不良影响，被认为对人类具有剧毒。山奈 (KMF) 是一种植物黄酮类化合物，具有显着的药理特性。本实验旨在评估 KMF 对 PQ 引起的大鼠心脏毒性的姑息作用。将24只大鼠随机分为4组，分别为对照组、毒物组（PQ处理组）、联合处理组（PQ+KMF）和KMF组。治疗 30 天后，百草枯中毒导致抗氧化酶活性显着降低，包括谷胱甘肽还原酶 (GSH)、谷胱甘肽 S-转移酶 (GST)、过氧化氢酶 (CAT)、谷胱甘肽过氧化物酶 (GPx)、超氧化物歧化酶 (SOD)和谷胱甘肽二硫化物还原酶 (GSR)，而活性氧 (ROS)、丙二醛 (MDA) 以及过氧化氢 (H 2 O 2 )_水平则_有所升高。此外，心脏损伤标志物、肌酐磷酸激酶 (CPK)、肌酸激酶-肌红蛋白结合 (CK-MB) 和乳酸脱氢酶 (LDH) 以及肌钙蛋白 I 的浓度因 PQ 治疗而增加。此外，炎症细胞因子如肿瘤坏死因子 α (TNF-α)、核因子-κ B (NF-κB)、白细胞介素 6 (IL-6)、白细胞介素 1 β (IL-1β) 和环氧合酶 - PQ 中毒组中 COX-2（COX-2）水平升高。PQ暴露降低了心脏抗凋亡标志物（Bcl-2）的基因表达，但凋亡标志物（caspase-9、caspase-3和Bax）的基因表达增加。在毒物（PQ）暴露组中也观察到组织病理学损伤。然而，KMF 的施用显着缓解了 PQ 引起的上述破坏。根据这些发现，得出的结论是，KMF 是一种有前途的生物活性化合物，由于其出色的抗氧化、抗凋亡、抗炎以及心脏保护潜力，可用作对抗 PQ 引起的心脏损伤的治疗剂。