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Background: Neuroinflammation plays a role in the pathogenesis of HIV-associated dementia (HIV). Activation of microglia is essential for triggering inflammatory-mediated neurotoxicity. HIV-1 120 kDa envelope glycoprotein (gp120) induces microglial NF-κB signaling which in turn induces proinflammatory and iNOS gene transcription. Continuous or excessive activation of NF-κB signaling leads to persistent production of TNF-α and nitric oxide by microglia and induces neuronal apoptosis. Alpha-pinene is a natural substance extracted from a pine tree and has efficacy in inhibiting NF-κB signaling. Objective: This study was designed as a true experimental study and aimed to investigate the effect of alpha-pinene administration toward inflammatory response represented by the percentage of microglia containing activated NF-κB and iNOS expression. Methods: Neuron-glia primary culture from brain tissue of rat fetus was divided into 5 groups as follows: negative control; positive control (gp120 1nM); treatment I, II, and III (gp120 1 nM + alphapinene 0.4 μg/mL, 2 μg/mL, and 10 μg/mL, respectively). Microglial NF-κB and iNOS expression were analyzed using the immunohistochemistry method. Neuronal apoptosis was measured by the TUNNEL method. Results: Results showed that alpha-pinene administration on gp120-treated neuron-glia at all dosages decrease NF-kB activation, iNOS expression, and apoptotic neuron significantly as compared to the gp120-only treated group (p<0.05). Furthermore, alpha-pinene did not affect NF-kB activation and neuronal apoptosis (p>0.05), but significantly elevate iNOS expression (p<0.05) mainly in dosage I and II. Conclusion: We concluded that alpha-pinene has neuroprotective effect on gp120-treated neuron-glia cells through modulation of NF-kB and iNOS expression thus inhibit neuronal apoptosis.

ALPHA-PINENE ATTENUATES MICROGLIAL NF-ΚB ACTIVATION AND INOS EXPRESSION IN GP120-INDUCED NEUROINFLAMMATION