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Journal : Narra J

Phytocompounds of Nigella sativa seeds extract and their neuroprotective potential via EGR1 receptor inhibition: A molecular docking study Kulsum, Kulsum; Syahrul, Syahrul; Hasbalah, Kartini; Balqis, Ummu
Narra J Vol. 3 No. 2 (2023): August 2023
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v3i2.173

Abstract

Bioactivity of Nigella sativa seed extract has the potential as a neuro-protector, offering its promising utility in the clinical setting for brain injury management. This study aimed to identify the phytocompounds contained in the extract of N. sativa seeds and further screen their respective neuronal anti-inflammatory activities in silico. The extract of N. sativa seeds was prepared through successive maceration using non-polar to polar solvents (n-hexane and ethanol, respectively). The phytocompounds in the ethanolic extract were initially identified through qualitative analysis and further analyzed with gas chromatography-mass spectrometry (GC-MS). The spectral data were compared with the compound library for identification. The identified phytocompounds were then simulated computationally for their binding affinities toward the active pocket of early growth response-1 (EGR1) receptor (PDB: 14r2a). We found that the ethanolic extract of N. sativa seeds were predominantly constituted of hexadecanoic acid, ethyl ester (17.15%); linoleic acid ethyl ester (15.0%); octadecanoic acid (13.26%); and ethyl oleate (10.38%). The binding affinity of the phytocompounds ranged from -7.49 kcal/mol (methyl palmitoleate) to -14.31 kcal/mol (9-hexadecanoic acid, methyl ester), with 12 compounds having binding affinity < -10 kcal/mol. In conclusion, ethanolic extract of N. sativa seeds are rich with fatty acids that have active as anti-inflammatory and may exert neuronal protection by inhibiting EGR1 receptor. Studies using animal models to confirm the activity are warranted.
Oxygen saturation profile in traumatic brain injury animal model after propofol administration Kulsum, Kulsum; Syahrul, Syahrul; Hasbalah, Kartini; Balqis, Ummu; Suryadi, Taufik
Narra J Vol. 3 No. 2 (2023): August 2023
Publisher : Narra Sains Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.52225/narra.v3i2.189

Abstract

Traumatic brain injury (TBI) is a traumatic that often leads to death due to untreatable cerebral hypoxia, indicated by oxygen saturation of <90%. Cerebral hypoxia is rarely monitored and thereby often overlooked as a cause of mortality and monitoring oxygen saturation is an accurate method to detect the condition. Propofol, an anesthetic agent, is commonly used in the management of TBI; however, its effect on brain tissue and cerebral hypoxia in TBI cases is not well understood. The aim of this study was to evaluate the profile of oxygen saturation in TBI animal model after propofol administration. A laboratory experimental study was conducted, involving 18 male Rattus novergicus rats (aged 4–8 weeks with weight between 150–200 grams) divided into three different treatment groups (non-TBI, TBI without propofol, and TBI with propofol). Oxygen saturation was measured regularly from day 1 to day 8 using pulse oximetry. The oxygen saturation percentages were compared between the TBI rats with and without propofol administration using independent Student t-rest. The results revealed significant reductions of oxygen saturation levels of animals within propofol-treated TBI group compared to that of the untreated-TBI group (p<0.05), with the average oxygen saturation ranging from 80.8%±6.96% vs 86.8%±5.48%. This finding suggests a reducing effect of propofol administration on oxygen saturation levels in rats with TBI and this potentially causes cerebral hypoxia.