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All Journal Universa Medicina Molecular and Cellular Biomedical Sciences (MCBS) Acta Biochimica Indonesiana Health and Medical Journal
Febriana Catur Iswanti
Department Of Biochemistry And Molecular Biology, Faculty Of Medicine, Universitas Indonesia, Jakarta
Biochemistry, Genetics & Molecular Biology Dentistry Health Professions Immunology & microbiology Medicine & Pharmacology Neuroscience Public Health

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The increased of carbonic anhydrase in liver tissue of rat induced by chronic systemic hypoxia Rahmawati Ridwan; Febriana Catur Iswanti; Mohamad Sadikin
Acta Biochimica Indonesiana Vol. 1 No. 1 (2018): 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.v1i1.1

Abstract

Background: Carbonic anhydrases (CAs) are metalloenzymes which catalyze the reversible hydration/dehydration reaction of CO2, in order to maintain the cell homeostasis. These enzymes are found in various tissues and involve in a number of different physiological processes, including ion transport, acid-base balance, bone formation, and gluconeogenesis. Objective: To examine the specific activity of CA and to observe the liver tissue respond to oxidative stress by measured the malondialdehyde (MDA) concentration, in rat liver tissue induced by chronic systemic hypoxia for 1, 3, 5, 7, and 14 days of hypoxia. Results: The study showed that the activity of CA induced by chronic systemic hypoxia significantly increasing at early exposure to the hypoxic condition, at day 1 and days 3 of hypoxia (0.281 and 0.262 nmol/mg protein/minute compared to control 0.155 nmol/mg protein/minute) (p<0.05). No statistical difference at treatments of hypoxia 5, 7, and 14 days. The concentration of MDA also increased significantly on day 3 of liver tissue hypoxia (0.013 nmol/mg compared to control 0.009 nmol/mg liver tissue) (p<0.05), and no statistical differences at day 1, 5, 7, and 14 days of hypoxia. Conclusion: There was damage of membrane cells affected by oxidative stress in the liver tissue of rats induced by chronic systemic hypoxia.
Correlation between malondialdehyde level and FOXO3 and CASP3 mRNA expression changed in early-onset preeclampsia placenta Ni Made Wiasty Sukanty; Febriana Catur Iswanti; Syarifah Dewi; Muhammad Faruqi; Alyssa Shafa Andiana; Ani Retno Prijanti
Acta Biochimica Indonesiana Vol. 4 No. 2 (2021): 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.61

Abstract

Background: Preeclampsia is one of the factors causing the high maternal mortality rate. The risk of morbidity and mortality is higher in Early Onset Preeclampsia (EOPE). Failure of spiral artery remodeling can cause oxidative stress that can inhibit placental development and increase trophoblast apoptosis. Objective: This study aims to analyze the oxidative stress and apoptosis of EOPE placentas. Methods: This study is an observational study with a cross-sectional design. A total of 31 EOPE placentas and 31 normal term placentas were used to measure the concentration of malondialdehyde (MDA) and the relative mRNA expression of FOXO3 and CASP3 using the spectrophotometric and RT-qPCR methods. Results: There was no difference in MDA concentration (p = 0.580) and FOXO3 (p = 0.467) and CASP3 (p = 0.243) mRNA expression in the normal and EOPE groups. There was a strong positive correlation between FOXO3 and CASP3 mRNA expression in the normal (p= 0.0001; r = 0.938) and EOPE groups (p = 0.0001; r = 0.855). There was no correlation between MDA concentration to FOXO3 (p = 0.124; r = 0.282) and CASP3 (p = 0.569; r = 0.106) mRNA expression in normal placenta. There was positive correlation between MDA concentration to FOXO3 (p = 0.016; r = 0.429) and CASP3 mRNA expression in EOPE placenta (p = 0.028; r = 0.395). Conclusion: These results indicate that cell integrity is still maintained through the autophagy process and the level of apoptosis in the EOPE placenta is regulated by ROS through FOXO3.
Innate Immune Response to House Dust Mite Allergens in Allergic Asthma Winna Soleha; Febriana Catur Iswanti
Molecular and Cellular Biomedical Sciences Vol 5, No 3 (2021)
Publisher : Cell and BioPharmaceutical Institute

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21705/mcbs.v5i3.217

Abstract

Asthma is a major health problem and one of the leading causes of death in the world. The prevalence of asthma in Indonesia is high, with a recurrence >50%. Allergic sensitization in asthma is mainly caused by house dust mite (HDM) allergens, both from the mite’s body and its contaminants (e.g., lipopolysaccharides). HDM allergens stimulate several pathways in the innate immune response based on the HDM allergen groups that sensitize them. The innate immune response to HDM allergen exposure occurs when pattern recognition receptors (PRRs) recognizes the allergen, thereby stimulating respiratory epithelial cells to release cytokines, namely, thymic stromal lymphopoietin (TSLP), interleukin-25 (IL -25), and IL-33. The release of IL-25 and IL-33 activates group 2 innate lymphoid cells (ILC2) to release Th2-type cytokines (i.e., IL-5 and IL-13), resulting in allergic airway inflammation via IgE secretion by B cells, recruitment of eosinophils, and respiratory tract remodeling. Dendritic cells induce an adaptive immune response through Th2 activation in the sensitization and effector phases. Other mediators that contributed to the innate immune response include C-C motif chemokine ligand 20 (CCL-20) and granulocyte-macrophage colony-stimulating factor (GM-CSF). A deeper understanding of the components and mechanisms involved in innate immunity against HDM allergens creates the potential to develop alternative therapeutic targets for allergic asthma treatment.Keywords: house dust mite allergens, innate immunity, allergic asthma, respiratory epithelium, inflammatory cytokines
Gut microbiome diversity as adjuvant marker for immune function Mahdaleny; Febriana Catur Iswanti
Acta Biochimica Indonesiana Vol. 5 No. 1 (2022): 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.80

Abstract

The gastrointestinal (GI) tract represents our most intimate contact with the external environment. The GI tract responsible for extracting the appropriate nutrients we need to thrive, maintaining an appropriate balance of helpful and harmful microbes, and acting as a conduit for waste removal. In essence, the extracellular matrix of gut mucosal biofilm is a complex network of microbes and their secretions, as well as the host's secretions and signals (mainly mucus/mucin). Mucin, bacterial polysaccharides, and protein combine to form a unique mucosal biofilm that serves as a home for a variety of commensal and pathogenic organisms in the host. Maintaining proper mucosal barrier function is vital for both GI and systemic health. The lumen of the gut contains numerous entities that should never reach the bloodstream or lymphatic system. The mucosal barrier's integrity is maintained by a single layer of tightly fitted columnar epithelial, and more than 70% of the immune system components are closely associated with the GI tract.
Chemokines in allergic asthma inflammation Sulfiana Sulfiana; Febriana Catur Iswanti
Universa Medicina Vol. 41 No. 3 (2022)
Publisher : Faculty of Medicine, Universitas Trisakti

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18051/UnivMed.2022.v41.289-301

Abstract

Asthma is the most frequent noncommunicable disease and one of the leading causes of years lived with disability. Asthma has a severe impact on a patient's life, being able to disturb the activities of both children and adults. The morbidity and mortality of asthma may depend on the severity and progressiveness of the symptoms experienced by the patient. Different and complex pathomechanisms underline the pathology of asthma, in which the regulation of innate and adaptive immune responses plays a role. There is a complex interaction between immune cells including chemokines involved in the pathogenesis of asthma. Immune cell trafficking is orchestrated by a family of small proteins called chemokines. Leukocytes express cell-surface receptors that bind to chemokines and trigger transendothelial migration. This review article outlines the main role of chemokines in inflammatory reactions that occur in allergic asthma, based on the latest literature studies that have been published previously. The allergic reaction in asthma expresses various chemokines and their receptors. Chemokines including eotaxins (CCL11, CCL24, and CCL26), CCL2, CCL5, CCL17, and CCL22 regulate immune cells that under pathological conditions travel to the inflammatory site, mainly in the lung, to protect the body from pathogen invasion. Chemokines are released by a number of immune cells such as monocytes, dendritic cells, mast cells, and epithelial cells in the airway. The biological effects of chemokine production are enhanced by secreted cytokines when an allergic reaction occurs in asthma, such as IL-4, IL-5, and IL-13. Chemokines cause an accumulation of different inflammatory cells at the site of inflammation, which ultimately results in tissue damage to the airway. The inhibition of the reactions evoked by the interaction between chemokines and their receptors is considered a candidate for the development of potent therapeutic drugs for asthma in the future.
Evasion of the Immune System by Mycobacterium tuberculosis: A Special Review on Macrophages Kurnia Maidarmi Handayani; Febriana Catur Iswanti
Health and Medical Journal Vol 6, No 2 (2024): HEME May 2024
Publisher : Universitas Baiturrahmah

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33854/heme.v6i2.1452

Abstract

Mycobacterium tuberculosis, the bacterium that caused tuberculosis, is estimated to affect 10 million people worldwide in 2019. This bacterium is an intracellular pathogen that is spread through the inhalation of bacterial aerosol particles. The innate immune system in the lungs is prepared to phagocytize these bacteria, particularly macrophages, dendritic cells, monocytes, and neutrophils. M. tuberculosis can evade attacks by the host immune system and has developed strategies to infect successfully, especially macrophages. This intracellular bacterium can inhibit phagolysosome fusion, which is associated with lipoarabinomannan (LAM) in the bacterial cell wall. M. tuberculosis also can persist in phagolysosomes by inhibiting acidification and also inhibiting the action of NOX2 from producing ROS. This ability also allows these bacteria to avoid autophagy within macrophages. Knowledge of the power of these bacteria to manipulate and evade the immune system, especially macrophages, is beneficial in developing medicines and vaccines in the future.
Co-Authors Alyssa Shafa Andiana Ani Retno Prijanti Arief Budi Witarto Halim, Abdul Istiqomah Agusta Kurnia Maidarmi Handayani Lusiyana Dwi Rahmawati Mahdaleny Mohamad Sadikin Mohamad Sadikin Muhammad Faruqi Ni Made Wiasty Sukanty Novi Silvia Hardiany Rahmawati Ridwan Reni Paramita Retno Wahyu Nurhayati Samsuridjal Djauzi Sulfiana Sulfiana Syarifah Dewi Tomohiko Yamazaki Winna Soleha