Cardioprotective effects of Dendrobium officinale polysaccharides on thiacloprid-induced cardiac injury via modulating mitochondrial dynamics.

Thiacloprid (THI), a widely used neonicotinoid pesticide, has been shown to induce cardiac injury, though the underlying mechanisms remain poorly understood. Dendrobium officinale polysaccharides (DOP), a bioactive compound with potent antioxidant properties, may offer protection against such toxicity. This study investigated the cardioprotective effects of DOP in THI-induced cardiac injury in quails, with a particular focus on the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Network pharmacology analysis identified key targets of DOP, linking them to oxidative stress, mitochondrial dysfunction, and inflammatory pathways. Experimental results demonstrated that DOP significantly reversed THI-induced hematological and biochemical abnormalities, including the restoration of cardiac biomarkers and mitigation of myocardial structural damage. DOP treatment notably activated the Nrf2 pathway, leading to the upregulation of antioxidant enzymes such as heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1), which countered THI-induced oxidative stress. Additionally, DOP restored mitochondrial dynamics by balancing mitochondrial fission and fusion proteins. These findings highlight the central role of Nrf2 activation in the cardioprotective effects of DOP, suggesting that DOP may serve as a promising therapeutic agent for mitigating pesticide-induced cardiovascular toxicity.