Neuroinflammation induced by activated microglia is a typical pathological feature in most neurodegenerative diseases. Generally, inhibition of neuroinflammation could attenuate damage of brain in neurodegenerative diseases. Photobiomodulation (PBM) has been proved to suppress neuroinflammation by decreasing microglial activation. However, the underlying mechanisms of PBM on microglial inflammation remain unclear. Herein, we studied the effects of mitochondrial function on PBM regulated microglial inflammation. The results showed that PBM attenuates lipopolysaccharide (LPS)-induced microglial proinflammatory response while ameliorating mitochondrial dysfunction. Further study revealed that PBM promotes mitophagy in microglia exposed to LPS. In addition, we found that 3- methyladenine (3-MA), the autophagy inhibitor, disrupts microglial mitophagy and reverses the protective effect of PBM on inflammation. Taken together, these studies underline the significance of mitophagy in suppressing inflammation and enhancing mitochondrial function in activated microglia under PBM treatment. Our research may supply a potential strategy to control the progression of neuroinflammation.
Morphine addiction causes major medical and social problems worldwide. Chronic morphine exposure results in the development of behavioral sensitization, accompanied by the disruption of brain homeostasis. As a key brain reward region, nucleus accumbens (NAc) plays a central role in brain reward mechanisms. Furthermore, neurons in NAc are impaired by chronic morphine abuse, but the contribution of morphine exposure to neurons is poorly understood. Here we indicated that morphine-induced an abnormal neuronal activation in NAc. Critically, we found a remarkable increase of mitochondrial fragmentation in neurons following burst activity. Taken together, these results define the effects of morphine on neurons in NAc, and provide a new insight for development of future morphine addiction therapeutics.
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