Abstract

Abstract Curcumin is a substance in turmeric root with anti-inflammatory, antioxidant, and anti-tumor properties, and has been widely used both as an herbal drug and a food additive to treat or prevent neurodisorders. To explore whether curcumin is able to treat HIV-associated neurocognitive disorders (HAND), we treated murine microglial cell line (N9) and primary rat cortical neurons with curcumin in the presence and absence of HIV gp120 (V3 loop) protein. We found that HIV gp120 profoundly induced N9 cells to produce reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1). HIV-1 gp120 also induced apoptosis of primary rat cortical neurons. Curcumin exerted powerful inhibitory effect against gp120-induced neuronal damage, reducing production of ROS, TNF-α and MCP-1 by N9 cells, and inhibiting apoptosis of primary rat cortical neurons. Curcumin may exert its biological activities through inhibition of gp120-mediated rectification and transient outward potassium current, as curcumin effectively reduced gp120-mediated elevation of potassium channel current of neurons. Conclusions: HIV gp120 increases ROS, TNF-α and MCP-1 production in microglia, and induces cortical neuron apoptosis by affecting the voltage-gated potassium channel current. Curcumin protects microglia and cortical neurons against HIV-mediated inflammation and apoptosis, probably through inhibition of gp120-induced elevation of the voltage-gated potassium current.

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