Oxidative stress is the pivot for PM2.5-induced lung injury.

Fine particulate matter (PM2.5) is a primary air pollutant recognized worldwide as a serious threat to public health. PM2.5, which has a diameter of less than 2.5 µm, is known to cause various diseases, including cardiovascular, respiratory, metabolic, and neurological diseases. Studies have shown that the respiratory system is particularly susceptible to PM2.5 as it is the first line of defense against external pollutants. PM2.5 can cause oxidative stress, which is triggered by the catalyzation of biochemical reactions, the activation of oxidases and metabolic enzymes, and mitochondrial dysfunction, all of which can lead to lung injury and aggravate various respiratory diseases including chronic obstructive pulmonary disease (COPD), asthma, pulmonary fibrosis, and cancer. Oxidative stress plays a crucial role in the harmful effects and mechanisms of PM2.5 on the respiratory system by activating several detrimental pathways related to inflammation and cellular damage. However, experimental studies have shown that antioxidative therapy methods can effectively cure PM2.5-induced lung injury. This review aims to clarify how PM2.5 induces oxidative stress and the mechanisms by which it is involved in the aggravation of various lung diseases. Additionally, we have listed antioxidant treatments to protect against PM2.5-induced lung injury.

Xanthohumol protect against acetaminophen-induced hepatotoxicity via Nrf2 activation through the AMPK/Akt/GSK3ß pathway.

OBJECTIVE: Acetaminophen (APAP) is one of the world's popular and safe painkillers, and overdose can cause severe liver damage and even acute liver failure. The effect and mechanism of the xanthohumol on acetaminophen-induced hepatotoxicity remains unclear. METHODS: The hepatoprotective effects of xanthohumol were studied using APAP-induced HepG2 cells and acute liver injury of mouse, seperately. RESULTS: In vitro, xanthohumol inhibited H2O2- and acetaminophen-induced cytotoxicity and oxidative stress. Xanthohumol up-regulated the expression of Nrf2. Further mechanistic studies showed that xanthohumol triggered Nrf2 activation via the AMPK/Akt/GSK3ß pathway to exert a cytoprotective effect. In vivo, xanthohumol significantly ameliorated acetaminophen-induced mortality, the elevation of ALT and AST, GSH depletion, MDA formation and histopathological changes. Xanthohumol effectively suppressed the phosphorylation and mitochondrial translocation of JNK, mitochondrial translocation of Bax, the activation o cytochrome c, AIF secretion and Caspase-3. In vivo, xanthohumol increased Nrf2 nuclear transcription and AMPK, Akt and GSK3ß phosphorylation in vivo. In addition, whether xanthohumol protected against acetaminophen-induced liver injury in Nrf2 knockout mice has not been illustated. CONCLUSION: Thus, xanthohumol exerted a hepatoprotective effect by inhibiting oxidative stress and mitochondrial dysfunction through the AMPK/Akt/GSK3ß/Nrf2 antioxidant pathway.