An essential characteristic of quantum dots (QDs) is their antimicrobial activity. Compared with conventional antibiotics, QDs not only possess photoluminescence properties for imaging and photodynamic therapy but also have high structural stability. To enhance their antimicrobial efficiency, QDs usually are functionalized by polymers, including poly(ethylene glycol), polyethyleneimine, and poly-l-lysine. Also, QDs conjugated with polymers, such as poly(vinylpyrrolidone) and polyvinylidene fluoride, are prepared as antimicrobial membranes. The main antimicrobial mechanisms of QDs are associated with inducing free radicals, disrupting cell walls/membranes, and arresting gene expression. The different mechanisms from traditional antibiotics allow QDs to play antimicrobial roles in multi-drug-resistant bacteria and fungi. Since the toxicity of the QDs on animal cells is relatively low, they have broad application in antimicrobial research as an effective alternative of traditional antibiotics.

Mitochondrial dysfunction is a major and common mechanism in developing nonalcoholic fatty liver disease (NAFLD). Replacement of dysfunctional mitochondria by functional exogenous mitochondria may attenuate intrahepatic excessive lipid and recover hepatocyte function. However, no data shows that mitochondria can be systemically administrated to animals to date. Here we suggest that mitochondria isolated from hepatoma cells are used as a mitotherapy agent to treat mouse fatty liver induced by high-fat diets. When the mitochondria were intravenously injected into the mice, serum aminotransferase activity and cholesterol level decreased in a dose-dependent manner. Also, the mitotherapy reduced lipid accumulation and oxidation injury of the fatty liver mice, improved energy production, and consequently restored hepatocyte function. The mitotherapy strategy offers a new potential therapeutic approach for treating NAFLD.

Rabies virus glycoprotein (RVG) peptides have been developed to deliver drugs for CNS diseases. In the present review, RVG-mediated drug delivery systems are summarised, which can deliver almost all small molecules and macromolecule agents.

Carbon tetrachloride (CCl₄)‐induced liver injury is predominantly caused by free radicals, in which mitochondrial function of hepatocytes is impaired, accompanying with the production of ROS and decreased ATP energy supply in animals intoxicated with CCl₄. Here we explored a novel therapeutic approach, mitochondrial transplantation therapy, for treating the liver injury. The results showed that mitochondria entered hepatocytes through macropinocytosis pathway, and thereby cell viability was recovered in a concentration‐dependent manner. Mitochondrial therapy could increase ATP supply and reduce free radical damage. In liver injury model of mice, mitochondrial therapy significantly improved liver function and prevented tissue fibrogenesis. Transcriptomic data revealed that mitochondrial unfold protein response (UPR^mt), a protective transcriptional response of mitochondria‐to‐nuclear retrograde signaling, would be triggered after mitochondrial administration. Then the anti‐oxidant genes were up‐regulated to scavenge free radicals. The mitochondrial function was rehabilitated through the transcriptional activation of respiratory chain enzyme and mitophage‐associated genes. The protective response re‐balanced the cellular homeostasis, and eventually enhanced stress resistance that is linked to cell survival. The efficacy of mitochondrial transplantation therapy in the animals would suggest a novel approach for treating liver injury caused by toxins.