| Abstrakt: |
aimuli Arozal,3 Hee Jae Lee,4 Agian Jeffilano Barinda,3,5 Yulvian Sani,6 Abdul Munim71Doctoral Program in Biomedical Science, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; 2Faculty of Medicine, Universitas Muhammadiyah Sumatera Utara, Medan, Indonesia; 3Department of Pharmacology and Therapeutics, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; 4Department of Pharmacology, School of Medicine, Kangwon National University, Chuncheon, Republic of Korea; 5Metabolic, Cardiovascular, and Aging Cluster, Indonesia Medical Education and Research Institute (IMERI), Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia; 6Research Center for Biomedical Research, National Research and Innovation Agency, Jakarta, Indonesia; 7Department of Pharmacognosy-Phytochemistry, Faculty of Pharmacy, Universitas Indonesia, Depok, West Java, IndonesiaCorrespondence: Wawaimuli Arozal, Department of Pharmacology and Therapeutics, Faculty of Medicine, Universitas Indonesia, Jl. Salemba Raya No. 6, Jakarta, Indonesia, 10430, Tel +62-21-31930481, Fax +62-21-3920947, Email [email protected] ; [email protected] Hee Jae Lee, Department of Pharmacology, School of Medicine, Kangwon National University, Chuncheon Campus 1, Gangwondaehakgil, Chuncheon-si, Gangwon-do, 24341, Republic of Korea, Tel/Fax +82-33-250-8850, Email [email protected] Purpose: Repeated stress events are well known to be associated with the onset of behavioral abnormalities including depression, anxiety and memory impairment. In spite of the traditional uses of Moringa oleifera (MO), no experimental evidence for its use against chronic stress exists. Here, we investigated whether seed oil from MO (MOO) could improve behavior abnormalities of chronic stress mice induced by water-immersion restraint stress (WIRS) and the underlying mechanism. Methods: BALB/C male mice at 12 weeks of age were exposed to chronic WIRS for two weeks and divided in to four groups: normal group, WIRS group, WIRS+MOO1 group (treated with MOO at the dose of 1 mL/kg BW), and WIRS+MOO2 group (treated with MOO 2 mL/kg BW). The MOO treatment was given orally for 23 days. On day 24, we checked the behavior parameters, the plasma level of cortisol, acetylcholinesterase (AChE) activity in hippocampus, mRNA expression level of brain-derived neurotrophic factor (BDNF) and oxidative stress parameters in brain tissues. In addition, we also checked the histopathological features of the gastric mucosa wall. Results: Administration of MOO ameliorated anxiety-like, depression-like and memory impairment phenotypes in the WIRS mouse model although the plasma cortisol concentrations were comparable among the groups. Of note, MOO both in two doses could suppress the AChE activity in hippocampus tissue and ameliorated the MDA level in prefrontal cortex tissue in mice exposed to WIRS. Although only WIRS+MOO2 group could increase the mRNA expression of BDNF, the histopathological gastric mucosa wall features were improved in all MOO groups. Conclusion: Taken together, these finding suggested that MOO may have a neuroprotective effect in the mouse model of WIRS as evidenced by improving the abnormal behaviors through enhancing mRNA expression level of BDNF, inhibited AChE activity, and prevented the increase of MDA level in the brain. [ABSTRACT FROM AUTHOR] |
