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Updated: Jun 14, 2026
Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures
Published on: July 25, 2022
Melatonin attenuates methamphetamine-induced overexpression of pro-inflammatory cytokines in microglial cell lines
Jiraporn Tocharus1, Chakkrapong Khonthun, Sukumal Chongthammakun
1Department of Biochemistry, Naresuan University, Phitsanulok, Thailand.
Abstract:
Methamphetamine (METH), the most commonly abused drug, has long been known to induce neurotoxicity. METH causes oxidative stress and inflammation, as well as the overproduction of both reactive oxygen species (ROS) and reactive nitrogen species (RNS). The role of METH-induced brain inflammation remains unclear. Imbroglio activation contributes to the neuronal damage that accompanies injury, disease and inflammation. METH may activate microglia to produce neuroinflammatory molecules. In highly aggressively proliferating immortalized (HAPI) cells, a rat microglial cell line, METH reduced cell viability in a concentration- and time-dependent manner and initiated the expression of interleukin 1beta (IL-1beta), interleukin 6 (IL-6) and tumor necrosis factor alpha. METH also induced the production of both ROS and RNS in microglial cells. Pretreatment with melatonin, a major secretory product of the pineal gland, abolished METH-induced toxicity, suppressed ROS and RNS formation and also had an inhibitory effect on cytotoxic factor gene expression. The expression of cytotoxic factors produced by microglia may contribute to central nervous system degeneration in amphetamine abusers. Melatonin attenuates METH toxicity and inhibits the expression of cytotoxic factor genes associated with ROS and RNS neutralization in HAPI microglia. Thus, melatonin might be one of the neuroprotective agents induced by METH toxicity and/or other immunogens.
Insights
Methamphetamine (METH) causes brain cell damage through inflammation and oxidative stress. Melatonin, however, protects against METH toxicity by reducing these harmful effects in microglial cells.
Area of Science:
- Neuroscience
- Toxicology
- Pharmacology
Background:
- Methamphetamine (METH) abuse is linked to neurotoxicity, involving oxidative stress and inflammation.
- Microglia activation plays a role in METH-induced neuronal damage, but the precise mechanisms are unclear.
Purpose of the Study:
- To investigate the effects of METH on microglial cells and the potential neuroprotective role of melatonin.
Main Methods:
- Using a rat microglial cell line (HAPI cells), researchers assessed METH's impact on cell viability, inflammatory marker expression (IL-1beta, IL-6, TNF-alpha), and reactive oxygen/nitrogen species (ROS/RNS) production.
- Melatonin's effects on METH-induced toxicity and related molecular changes were evaluated.
Main Results:
- METH reduced microglial cell viability and increased the expression of pro-inflammatory cytokines and ROS/RNS.
- Melatonin pretreatment effectively counteracted METH-induced toxicity, suppressed ROS/RNS generation, and inhibited cytotoxic factor gene expression.
Conclusions:
- METH-induced microglial activation and subsequent neuroinflammation contribute to central nervous system degeneration.
- Melatonin demonstrates significant neuroprotective potential against METH toxicity by neutralizing ROS/RNS and inhibiting inflammatory pathways.
