MECHANISM OF SOLANUM BETACEUM TO PREVENT MEMORY IMPAIRMENT IN CIGARETTE SMOKE-EXPOSED RAT

SITI KHAERUNNISA; KURNIA KUSUMASTUTI; ARIFA MUSTIKA; NANIK SITI AMINAH; SUHARTATI SUHARTATI

doi:10.22159/ijap.2019.v11s3.M1024

Authors

SITI KHAERUNNISA Departement of Medical Biochemistry, Faculty of Medicine, Universitas Airlangga, Indonesia.
KURNIA KUSUMASTUTI Departement of Neurology, Universitas Airlangga -Dr. Soetomo Hospital, Indonesia.
ARIFA MUSTIKA Departement of Medical Pharmacology, Faculty of Medicine, Universitas Airlangga, Indonesia.
NANIK SITI AMINAH Departement of Chemistry, Faculty of Medicine, Universitas Airlangga, Indonesia.
SUHARTATI SUHARTATI Departement of Medical Biochemistry, Universitas Wijaya Kusuma, Indonesia.

DOI:

https://doi.org/10.22159/ijap.2019.v11s3.M1024

Keywords:

Solanum betaceum, N-methyl-D-aspartate, c-AMP response element binding, Brain-derived neurothropic factor, Neuron, Glia, Memory

Abstract

Objective: The aim of this study was conducted to evaluate the neuroprotective role of Solanum betaceum against memory impairment due to chronic cigarette smoke exposure in rat brain.

Methods: Adult male albino rats were exposed to cigarette smoke for 28 days, 3 pc cigarette/day, and simultaneously administered with S. betaceum in Groups K2, K3, and K4 (100 mg/kg b.w/day, 200 mg/kg b.w/day, and 400 mg/kg b.w/day), respectively. The level of N-methyl-D-aspartate (NMDA), c-AMP response element binding (CREB) protein, brain-derived neurotrophic factor (BDNF), number of neuron and glial cells, and memory was also measured.

Results: S. betaceum administration could prevent from memory impairment significantly (p<0.05) by decreased time to reach the target at Y-Maze and maintained the levels of CREB, BDNF, neuron, and glial cells (microglia, astrocytes, and oligodendrocytes) significantly (p<0.05) but did not significantly decreased NMDA levels (p>0.05).

Conclusion: Exposure to cigarette smoke compromised the memory functions. The result of this study shown that administration of S.betaceum could inhibit memory impairment and inhibit the decrease of neuron cells , increase the level of BDNF and number of glia cells including microglia, astrocytes and oligodendrocytes. The mechanism of S. betaceum to prevent memory impairment through activation of CREB (the transcription factor) which further enhances the formation of BDNF (the neurotrophic factors), thus increase activation of the glia cells to protect brain cell damage, thus preventing memory impairment due to cigarette smoke exposure.

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