Publikasi Scopus FKUI Tahun 2010 s/d 2020 (data Per 3 Februari 2021)

Syam A.F., Simadibrata M., Wanandi S.I., Hernowo B.S., Sadikin M., Rani A.A.
Gastric ulcers induced by systemic hypoxia.
Acta medica Indonesiana
Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jakarta Pusat, Indonesia
Syam, A.F., Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jakarta Pusat, Indonesia; Simadibrata, M.; Wanandi, S.I.; Hernowo, B.S.; Sadikin, M.; Rani, A.A.
to assess the effect of systemic hypoxia on gastric mucosa and the activation of stress-responsive transcription factors induced by hypoxia. in this experimental study, rats were allocated to control and experimental groups. The experimental group was divided into subgroups and subjected to hypoxia conditions for 1, 7, 14 or 21 days. Afterwards, histopathological evaluation and study of the protein expression of the gastric mucosa were performed. the results showed that longer exposure to hypoxic conditions leads to more severe gastric ulceration. Twenty-four hours after induction, 60% of rats had developed gastric ulcers. Seven days after induction, 80% of rats developed gastric ulcers. In the 14-day and 21-day hypoxia conditions, epithelialization (a sign of gastric ulcer healing) was observed. Evaluation of the average ulcer depth on the day of treatment showed that the greatest depth was on day 7, and the shallowest was on day 21 of treatment. Western blot analyses demonstrated that systemic hypoxia resulted in the expression of heat shock factor (HSF) and heat shock protein 70 (HSP-70), which were highest on day 7 and then regressed gradually. In control, HSF-1 and HSP-70 were not detected by Western blot analysis in the control group (normoxia). in this study, systemic hypoxia caused gastric ulcers, and during the time of exposure to hypoxia, an adaptation process in the form of gastric epithelialization occurred in the rats. This development of gastric lesions was in line with the expression pattern of HSF-1 HIF-1 and HSP-70.
heat shock protein 70; hypoxia inducible factor 1alpha; oxygen; adaptation; animal; anoxia; article; cell protection; disease model; epithelium cell; genetics; male; metabolism; pathophysiology; physiological stress; rat; secretion; Sprague Dawley rat; stomach acid; stomach mucosa; stomach ulcer; time; wound healing; Adaptation, Physiological; Animals; Anoxia; Cytoprotection; Disease Models, Animal; Epithelial Cells; Gastric Acid; Gastric Mucosa; HSP70 Heat-Shock Proteins; Hypoxia-Inducible Factor 1, alpha Subunit; Male; Oxygen; Rats; Rats, Sprague-Dawley; Stomach Ulcer; Stress, Physiological; Time Factors; Wound Healing

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