ABSTRACT
Methamphetamine abuse and HIV infection are extremely serious public health and social problems facing the world today. Methamphetamine and HIV-1 Tat protein can induce neurotoxicity in an individual and synergistic way, and neuroinflammation is one of the most important mechanisms for ca-using neurotoxicity. Neuroinflammation can be mediated by glial cells, cytokines, NLRP3 inflammasomes, etc. This paper reviews the research progress of neuroinflammation induced by methamphetamine and HIV-1 Tat protein in recent years, with the aim of providing reference and basis for further exploration of the mechanisms of neuroinflammation caused by them and effective drug intervention targets in the future.
ABSTRACT
At present, METH has surpassed the traditional illegal psychoactive substances and become the most widely abused illegal psychostimulant in China.Endoplasmic reticulum ( ER) plays an important role in regulating the normal physiological functions of various cells by virtue of its strong membrane strnc- ture and a large number of enzymes on the membrane.Endoplasmic reticulum stress ( ERS) is a series of adaptive responses made by cells when ER homeostasis is destroyed.When ERS occurs, it will drive the activation of unfolded protein response (I PR ) , which aims to protect cells from stress, reduce biosyn- thetic load and help to rebuild cell homeostasis.Persistent ERS will further aggravate the pressure of ER and induce cell death by using UPR signaling pathway.'Hie neurotoxicity induced by METH is closely related to ERS.This paper elaborates on ERS and UPR signaling pathway, and summarizes the relationship between ERS.apoptosis and autophagy, so as to provide new ideas and potential therapeutic targets for the basic research and prevention of METH induced neurotoxicity mechanism.