TY - JOUR
T1 - Mechanism of Solanum betaceum to prevent memory impairment in cigarette smoke-exposed rat
AU - Khaerunnisa, Siti
AU - Kusumastuti, Kurnia
AU - Mustika, Arifa
AU - Aminah, Nanik Siti
AU - Suhartati, Suhartati
N1 - Funding Information:
This research was supported by Universitas Airlangga, Surabaya, East Java, Indonesia, and Lembaga Pengelola Dana Keuangan, Ministry of Finance Republic of Indonesia.
Publisher Copyright:
© 2019 The Authors. Published by Innovare Academic Sciences Pvt Ltd.
PY - 2019/7
Y1 - 2019/7
N2 - 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.
AB - 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.
KW - Brain-derived neurothropic factor
KW - C-AMP response element binding
KW - Glia
KW - Memory
KW - N-methyl-D-aspartate
KW - Neuron
KW - Solanum betaceum
UR - http://www.scopus.com/inward/record.url?scp=85071706180&partnerID=8YFLogxK
U2 - 10.22159/ijap.2019.v11s3.M1024
DO - 10.22159/ijap.2019.v11s3.M1024
M3 - Article
AN - SCOPUS:85071706180
SN - 0975-7058
VL - 11
SP - 25
EP - 29
JO - International Journal of Applied Pharmaceutics
JF - International Journal of Applied Pharmaceutics
ER -