Yongjie Zhang,Shulin He,Chengyin He,Ling Zhou,Ou Xu,Liang Qiao,Bin Chen,Yueqing Cao,Zhengbo He
The use of insecticides, primarily pyrethroids, is a pivotal strategy for mosquito control globally. Bioallethrin, the first commercially available volatile pyrethroid, can elicit spatial (i.e., noncontact) repellency to mosquitoes through the coactivation of olfactory receptor neurons and sodium channels. However, the olfactory mechanism of the repellency elicited by bioallethrin in mosquitoes is still unclear. Here, we demonstrated the involvement of AsOBP1 in the bioallethrin repellency in Anopheles sinensis , one of the main vectors of vivax malaria in China and other Southeast Asian countries. The behavioral and electrophysiological analyses in AsOrco −/− mutant found that the spatial repellency elicited by bioallethrin depended on the odorant receptor (OR)-mediated olfactory pathway. Furthermore, the repellency was reduced in the AsOBP1 −/− mutant and a pyrethroid-resistant strain, in which the expression of AsOBP1 was significantly decreased. Moreover, recombinant AsOBP1 protein bound to bioallethrin in an in vitro competition assay. These results indicate that activation of the AsOBP1 -mediated olfactory pathway is an important component of bioallethrin repellency. Our research lays the foundation for further elucidation into the olfactory mechanism of bioallethrin repellency and the behavioral modifications of pyrethroid-resistant mosquitoes.
Wang Deping,Li Bowen,Wang Shuchao,Hao Yingjian,Wang Hua,Sun Wei,Cao Jimin,Zhou Xin,Zheng Bin
Mitochondrial dysfunction and subsequent accumulation of reactive oxygen species (ROS) are key contributors to the pathology of ischemic cerebrovascular disease. Therefore, elimination of ROS and damaged mitochondria is crucial for the effective treatment of this disease. For this purpose, we designed an inhalation nanotherapeutic agent, P/D@Mn/Co 3 O 4 , to treat ischemic cerebrovascular disease. Mn/Co 3 O 4 effectively removed excess ROS from cells, reduced acute cellular oxidative stress, and protected neural cells from apoptosis. Furthermore, it depleted the H + surrounding mitochondria and depolarized the mitochondrial membrane potential, inducing mitophagy and eliminating abnormal mitochondria, thereby avoiding the continuous overproduction of ROS by eliminating the source of ROS regeneration. On intranasal administration, Mn/Co 3 O 4 encapsulated by platelet membranes and 2,3-(dioxy propyl)-trimethylammonium chloride can bypass the blood–brain barrier, enter the brain through the trigeminal and olfactory pathways, and target inflammatory regions to remove ROS and damaged mitochondria from the lesion area. In rat models of stroke and vascular dementia, P/D@Mn/Co 3 O 4 effectively inhibited the symptoms of acute and chronic cerebral ischemia by scavenging ROS and damaged mitochondria in the affected area. Our findings indicate that the nanotherapeutic agent developed in this study can be used for the effective treatment of ischemic cerebrovascular disease.
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