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All Journal HAYATI Journal of Biosciences Jurnal Biotek Medisiana Indonesia The Indonesian Biomedical Journal Universa Medicina Argipa (Arsip gizi dan Pangan) Indonesian Journal of Obstetrics and Gynecology (Majalah Obstetri dan Ginekologi Indonesia) Acta Biochimica Indonesiana Jurnal Ilmu Kefarmasian Indonesia Majalah Kesehatan Pharmamedika Bioscientia Medicina : Journal of Biomedicine and Translational Research Indonesian Archives of Biomedical Research (InABR) Makara Journal of Science Proceedings Book of International Conference and Exhibition on The Indonesian Medical Education and Research Institute
Ani Retno Prijanti
Departemen Biokimia Dan Biomolekuler Fakultas Kedokteran Universitas Indonesia
Agriculture, Biological Sciences & Forestry Biochemistry, Genetics & Molecular Biology Earth & Planetary Sciences Health Professions Immunology & microbiology Medicine & Pharmacology Neuroscience Public Health

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Higher HIF-1alpha Level in Cervical Cancer Worsen the Outcome of Radiotherapy in Stage IIIB Squamous Cell Carcinoma of the Cervix Malano, Yoarva; Fitriyadi Kusuma; Prijanti, Ani Retno; Winarto, Hariyono; Anggraeni, Tricia Dewi; Utami, Tofan Widya; Adiyarianni, Ghina
Indonesian Journal of Obstetrics and Gynecology Volume 12 No. 2 April 2024
Publisher : Indonesian Socety of Obstetrics and Gynecology

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.32771/inajog.v12i2.1871

Abstract

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.
The Increase in CD14+CD16+ Monocytes is Correlated with Cardiovascular Disease Risk Marker in Type 2 Diabetes Hikmat, Ujang Saeful; Prijanti, Ani Retno; Wibowo, Heri; Sukmawati, Indriyanti Rafi; Tahapary, Dicky Levenus
The Indonesian Biomedical Journal Vol 16, No 1 (2024)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v16i1.2798

Abstract

BACKGROUND: Type 2 Diabetes (T2D) impairs the innate immune system including monocytes. Monocytes are divided into two subgroups depending on the expression of cluster of differentiation (CD)14 and CD16 receptors, namely CD14+CD16- and CD14+CD16+. CD14+CD16+ are proinflammatory monocytes and develop into M1 type macrophages, which contribute to foam cell production, a risk factor for cardiovascular disease (CVD). Therefore, it is important to determine the influence of T2D conditions on changes in monocyte subsets and whether these changes correlate with CVD risk markers.METHODS: Peripheral blood mononuclear cell (PBMC) was obtained from 10 T2D subjects and 10 healthy donors. Subsequently, PBMC was incubated for 24 hours with and without 10 mL lipopolysaccharide. Flow cytometry was used to evaluate CD14 and CD16 expression, while multiplex immunoassays were applied to measure interleukin (IL)-1b and IL-10 concentrations in supernatants.RESULTS: In T2D, the percentage of CD14+CD16+ monocytes increased (p=0.07), and an increase in CD14+CD16+ monocytes more than 6.8% was linked with CVD risk markers (r=10.146, p=0.002). Meanwhile, inflammatory mediators released by monocytes shown an increase in IL-1b (p=0.041) but not in IL-10 (p=0.082) in T2D subjects. Fasting blood glucose levels were also found to be substantially linked with an increase in CD14+CD16+ monocytes (r=0.530, p=0.016).CONCLUSION: T2D patients had a higher percentage of CD14+CD16+ monocytes and IL-1b levels than healthy donors. An increase in CD14+CD16+ monocytes above 6.8% associated with CVD risk markers in T2D patients.KEYWORDS: type 2 diabetes, monocytes, CD14, CD16, cardiovaskular disease risk marker
The Effects of Vitamin E Administration in Non-Alcoholic Fatty Liver Disease Handayani, Tri; Prijanti, Ani Retno
Bioscientia Medicina : Journal of Biomedicine and Translational Research Vol. 8 No. 1 (2024): Bioscientia Medicina: Journal of Biomedicine & Translational Research
Publisher : HM Publisher

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37275/bsm.v8i1.909

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a liver disease which has high prevalence in the society. There is no drug that is considered to be able to effectively treat this disease until today. The treatments has wide range from modifications to diet and exercise. The role of vitamin E in the treatment of NAFLD has been studied in many researches. It has high antioxidant capacity that have the ability to decrease the level of reactive oxygen species (ROS) and prevent oxidative damage that can cause cellular senescence and apoptosis. The antioxidant properties may inhibit the progression into liver damage and may even treat hepatic fibrosis in NAFLD. It also has an anti-inflammatory role that affects various inflammatory cytokines produced in NAFLD. The use of vitamin E in non-alcoholic steatohepatitis without diabetes is advised by recent guidelines from the American Association for Study of Liver Disease (AASLD) and the European Association for the Study of Liver Disease (EASLD). In patients with non-alcoholic steatohepatitis, vitamin E can decrease oxidative stress, inhibit the pathogenesis of the disease, and be used as a therapeutic option. However, new research on the safety and efficacy of vitamin E in treating diabetic non-alcoholic steatohepatitis patients is still deemed insufficient.
Proteostasis disruption under hypoxia: therapeutic targets in cancer and neurodegenerative diseases Susi Rahmiyati; Ani Retno Prijanti; Sri Widia A Jusman; Syarifah Dewi
Acta Biochimica Indonesiana Vol. 8 No. 2 (2025): Acta Biochimica Indonesiana
Publisher : Indonesian Society for Biochemistry and Molecular Biology

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.32889/actabioina.142

Abstract

Proteostasis, the integrated network regulating protein synthesis, folding, trafficking, and degradation, is essential for cellular function and organismal health. Reduced oxygen availability disrupts proteostasis through increased reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, impaired ATP-dependent protein folding, and altered chaperone expression. In cancer, tumor cells exploit chronic unfolded protein response (UPR) signaling to enhance survival, angiogenesis, and therapeutic resistance. Inhibition of IRE1α and PERK pathways has shown efficacy in preclinical models, though clinical translation faces challenges including off-target toxicity. In neurodegenerative diseases—Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis—chronic hypoxia accelerates protein aggregate accumulation through oxidative modifications and impaired autophagy-lysosome function. Therapeutic strategies targeting γ-secretase, BACE1, and protein clearance pathways have demonstrated limited clinical success despite mechanistic rationale. Understanding hypoxia-induced proteostasis failure may inform therapeutic development, though significant obstacles remain in translating preclinical findings to effective treatments for cancer and neurodegenerative diseases.
Co-Authors AA Hawali Adiyarianni, Ghina Alyssa Shafa Andiana Andriani Andriani Andrijono Andrijono Andrijono Andrijono Bambang Sutrisna Dalilati, Annia Zhafarina Desak Gede Budi Krisnamurti Dian Ratih Laksmitawati Dicky Levenus Tahapary Fadilah Fadilah Fadilah Fadilah, Fadilah Febriana Catur Iswanti Ferry Sandra Fitriyadi Kusuma Frans D Suyatna Frans Ferdinal Hariyono Winarto Helmi Rizal Heri Wibowo Hikmat, Ujang Saeful Ika Superti Daruningrum Inawati Wanandi, Septelia Jusman, Sri Widia Azraki Jusman, Sri Widia Azraki Kenny Cantika Abadi Laila Nuranna Liem, Isabella Kurnia Linda Herlina Luh Putu Ratna Sundari M. Rafi Malano, Yoarva Mohamad Sadikin Mohamad Sadikin Mohamad Sadikin Muhamad Arif Budiman Muhammad Faruqi Ni Made Wiasty Sukanty Ninik Mudjihartini Novientri, Gissi Purba, Hastuti Handayani S Reni Paramita Riyadh Firdaus Rizka Ramadhani Rozana Nurftri Yulia Sadikin, Abdul Halim Sri Mutya Sekarutami Sri Widia A Jusman Susi Rahmiyati Syarifah Dewi Tjam Diana Samara Tri Handayani Tricia Dewi Anggraeni Utami, Tofan Widya Victor Tambunan Wawan Mulyawan Werdhasari, Asri Yurika Sandra