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Reactive oxygen species (ROS)-induced neuronal mitochondrial dysfunction is a key pathologic factor in sporadic Alzheimer's disease (AD). Neuronal mitochondria have been proposed to be a promising therapeutic target for AD, especially for the failures of phase III clinical trials on conventional amyloid-β (Aβ) targeted therapy. However, the efficient intravenous delivery of therapeutic agents to neuronal mitochondria in the brain remains a major challenge due to the complicated physiological environment. Recently, biomaterials-based nanomedicine has been widely investigated for the treatment of AD. Herein, we devised a strategy for functional antioxidant delivery to neuronal mitochondria by loading antioxidants into red blood cell (RBC) membrane-coated nanostructured lipid carriers (NLC) bearing rabies virus glycoprotein (RVG29) and triphenylphosphine cation (TPP) molecules attached to the RBC membrane surface (RVG/TPP NPs@RBCm). With the advantage of suitable physicochemical properties of NLC and unique biological functions of the RBC membrane, RVG/TPP NPs@RBCm are stabilized and enabled sustained drug release, providing improved biocompatibility and long-term circulation. Under the synergistic effects of RVG29 and TPP, RVG/TPP NPs@RBCm can not only penetrate the blood–brain barrier (BBB) but also target neuron cells and further localize in the mitochondria. After encapsulating Resveratrol (RSV) as the model antioxidant, the data demonstrated that RVG/TPP-RSV NPs@RBCm can relieve AD symptoms by mitigating Aβ-related mitochondrial oxidative stress both in vitro and in vivo. The memory impairment in APP/PS1 mice is significantly improved following the systemic administration of RVG/TPP-RSV NPs@RBCm. In conclusion, intravenous neuronal mitochondria-targeted dual-modified novel biomimetic nanosystems are a promising therapeutic candidate for ROS-induced mitochondrial dysfunction in AD. [ABSTRACT FROM AUTHOR]

Emamectin benzoate (EMB) is one of the high-efficacious pesticide commonly used to control the ferocious economic crop pest S. exigua in the field. The results of S. exigua life table treated with three lethal doses of EMB (LC5, LC20 and LC50) indicated that three lethal doses of EMB could all inhibited the proliferation of S. exigua population effectively by long-lasting inhibit the survival of the S. exigua larvae and per female fecundity significantly (p < 0.05), and the inhibition effects of key life parameters were affected by EMB stress in a dose-dependent manner. 67,123 unigenes with an N50 value of 1941 bp were assembled by RNA-seq data analyses and 44,113 were expressed more than 12 samples. Furthermore, 3517, 3139 and 5135 differentially expressed genes were identified under different lethal doses of EMB treatment. Finally, 16 hub genes and three olfaction-related genes were identified by WGCNA analysis as biomarkers for the EMB response, and the cAMP-dependent proteins, P450 metabolic-related genes and ABC transporter genes might have been involved in response to EMB stress in S. exigua. [ABSTRACT FROM AUTHOR]