Abstract

Angiostrongylus cantonensis, which is also known as rat lungworm, is an important food-borne zoonotic parasite that causes severe neuropathological damage and symptoms, including eosinophilic meningitis and eosinophilic meningoencephalitis, in humans. At present, the therapeutic strategy for cerebral angiostrongyliasis remains controversial. Benzaldehyde, an important bioactive constituent of Gastrodia elata (Tianma) reduces oxidative stress by inhibiting ROS production. This study aimed to evaluate the therapeutic effect of benzaldehyde in combination with albendazole on angiostrongyliasis in animal models. First, the data from body weight monitoring and behavioural analyses demonstrated that benzaldehyde improve body weight and cognitive function changes after A. cantonensis infection. Next, blood‒brain barrier breakdown and pathological changes were reduced after benzaldehyde and albendazole treatment in A. cantonensis-infected BALB/c mice. Subsequently, we established four RNA-seq datasets from different treatment mouse brains, including the normal, infection, infection+albendazole, and infection+albendazole+3-HBA groups. Ultimately, we found that benzaldehyde regulates cell apoptosis, oxidative stress, and sonic hedgehog signalling in A. cantonensis-infected mouse brains. This study evaluated the therapeutic effect of benzaldehyde on angiostrongyliasis and provided a potential therapeutic strategy for human angiostrongyliasis in the clinic. Moreover, we elucidated the molecular mechanism of benzaldehyde in A. cantonensis-infected mouse brains.

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