Thiacloprid (THI) is a neonicotinoid insecticide, and its wide-ranging use has contributed to severe environmental and health problems. Dendrobium officinale polysaccharide (DOP) possesses multiple biological activities such as antioxidant and antiapoptosis effect. Although present research has shown that THI causes kidney injury, the exact molecular mechanism and treatment of THI-induced kidney injury remain unclear. The study aimed to investigate if DOP could alleviate THI-induced kidney injury and identify the potential molecular mechanism in quails. In this study, Japanese quails received DOP (200 mg/kg) daily with or without THI (4 mg/kg) exposure for 42 days. Our results showed that DOP improved hematological changes, biochemical indexes, and nephric histopathological changes induced by THI. Meanwhile, THI exposure caused oxidative stress, apoptosis, and autophagy. Furthermore, THI and DOP cotreatment significantly activated the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway, restored antioxidant enzyme activity, and reduced apoptosis and autophagy in quail kidneys. In summary, our study demonstrated that DOP mitigated THI-mediated kidney injury was associated with oxidative stress, apoptosis, and autophagy via activation of the Nrf2/HO-1 signaling pathway in quails.
Keywords: Dendrobium officinale polysaccharide; apoptosis; autophagy; oxidative stress; thiacloprid.
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