Effects of Melissa Officinalis L. Leaves Ethanolic Extract on LPS-Induced Neuroinflammation in Rat Brain
- سال انتشار: 1398
- محل انتشار: سومین همایش بین المللی التهاب سیستم عصبی و سومین فستیوال دانشجویی علوم اعصاب
- کد COI اختصاصی: NIMED03_132
- زبان مقاله: انگلیسی
- تعداد مشاهده: 444
نویسندگان
Student Research Committee, Birjand University of Medical Sciences, Birjand, Iran
Cellular and Molecular Research Center, Department of Anatomy, Birjand University of Medical Sciences, Birjand, Iran
چکیده
During the last decade, lemon balm (Melissa officinalis L.) has attracted an increased interest due to its experimentally proven beneficialeffects on many neurological disorders such as cognitive impairment, insomnia, anxiety, and stress. The aim of this study was to elucidate the possible mechanistic inflammatory-modulatory effects of Melissa officinalis L. leaves ethanolic extract (MO) on Lipopolysaccharide(LPS)-induced neuroinflammation in rat brain. Materials and Methods: Neuroinflammation was induced by intracerebroventricular (ICV) injection of LPS (50 μg/20μl; 10 μl injected to each ventricle) dissolved in artificial cerebrospinal fluid (CSF) using stereotaxic apparatus in adult male Wistar rats (n=15); whereas, a control group (n=5) only received artificial CSF (ICV). MO extract at the doses of 50, and 100 mg/kgwas intraperitoneally administrated to the experimental groups 30 min before LPS injection and continued once per day for 9 days. At the ninth day, the rats were sacrificed, perfused by cold saline through their hearts, and their brains were carefully collected, promptlydissected into cerebral cortex (CC) and hippocampus (HIP). The samples were homogenized, sonicated, centrifuged and their supernatants were collected. The cytokines including tumor necrosis factor alpha (TNF-α) and Interleukin 1 beta (IL-1β) were estimated using ELISA kits. Results: Compared to control group, ICV injection of LPS significantly increased TNF-α, and IL- 1β in both of HIP and CC parts. MO treatment (both doses) could effectively normalized TNF-α at both CC and HIP regions. However, MO treatment only at the maximum dose (100mg/kg) significantly decreased IL- 1β just in CC compared to neuroinflammation model group; whereas, it could not significantly ameliorate IL-1β in HIP. Conclusion: To the best of our knowledge, the data of this study for the first time provide evidence that inflammatory-modulatory mechanism may be involve in neuroprotective potential of MO and could be adhered in further mechanistic studies.کلیدواژه ها
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