Claim Missing Document
Check
Articles

Found 2 Documents
Search

Intermittent Hypobaric Hypoxia Preconditioning Ameliorates Kidney Damage Compared to Acute Hypoxia Sadikin, Abdul Halim; Jusman, Sri Widia Azraki; Mulyawan, Wawan; Prijanti, Ani Retno
HAYATI Journal of Biosciences Vol. 32 No. 6 (2025): November 2025
Publisher : Bogor Agricultural University, Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.4308/hjb.32.6.1437-1446

Abstract

Many studies have reported that intermittent hypobaric hypoxia (IHH) can cause oxidative stress and tissue damage in the kidneys, which can lead to impaired kidney function. However, a study using simulated intermittent hypobaric hypoxia was considered to have a protective role for the kidneys. This study aims to determine the effect of IHH on kidney adaptation to oxidative stress and kidney damage. Twenty-five rats were divided into five groups: control, one-time hypoxia (AHH), two-time hypoxia (IHH 1), three-time hypoxia (IHH 2), and four-time hypoxia (IHH 3). The intermittent interval was one week, and at the time of treatment, the rats were placed in a hypoxic chamber. At the end of treatment, the rats were sacrificed, and the kidneys, urine, and blood were collected. The kidney tissues were used for protein assay, ELISA (HIF-1α and VEGF), qPCR (cytoglobin (Cygb) and renin), SOD and GPx activity assay. Blood was used for creatinine and urea assay, and urine was used for KIM-1 ELISA. Formalin-submerged tissues were used for histopathological analysis. The level of HIF-1α and VEGF increased significantly from AHH to IHH 1. Cygb and renin expressions peaked at AHH and decreased at subsequent IHH groups. The Nrf2 level and GPx activity didn’t show any difference, but SOD activity peaked at IHH 1. The creatinine level only peaked at IHH 2; other groups remained the same as the control. Urea levels decreased with more IHH sessions, and KIM-1 didn’t show any difference. Our findings exhibit that hypoxia preconditioning by IHH treatment leads to the kidney’s adaptability to hypoxia and does not cause kidney damage.
Hyperbaric Oxygen Therapy for Traumatic Brain Injury: A Review Of History, Development, Current Techniques, and Future Directions Wiwoho, Yudi Yuwono; Sadikin, Abdul Halim; Jusuf, Ahmad Aulia; Mulyawan, Wawan; Mudjihartini, Ninik; Ibrahim, Nurhadi; Jusman, Sri Widia A.; Sadikin, Mohamad
Proceedings Book of International Conference and Exhibition on The Indonesian Medical Education Research Institute Vol. 9 No. - (2025): Proceedings Book of International Conference and Exhibition on The Indonesian M
Publisher : Writing Center IMERI FMUI

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.69951/proceedingsbookoficeonimeri.v9i-.321

Abstract

Hyperbaric oxygen therapy (HBOT) has gained increasing attention as a potential adjunctive treatment for traumatic brain injury (TBI) patients. This narrative review discusses the historical background, current preclinical and clinical studies, and explores its underlying mechanisms from biomolecular, histological, and clinical perspectives. HBOT promotes neural recovery by improving oxygenation, preserving mitochondrial integrity, enhancing neurotrophic support and synaptic connectivity, mitigating secondary injury pathways (including oxidative stress, inflammation, and apoptosis), and promoting angiogenesis and vascular stability. These mechanisms have demonstrated improvements of motor, cognitive, and memory functions both in preclinical and clinical studies, although outcomes and treatment protocols vary. However, challenges remain regarding optimal protocols, patient selection, and adverse effects. Further high-quality clinical trials are required to define the optimal HBOT regimen are required.