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D018- Peran Vitamin D Pada Sel Epitel Paru A549 Untuk Mengurangi Sitokin Inflamasi (NF-kB, TNF-α, IL-Iβ, IL-6, IL-12) Sebagai Model Pada Sindrom Gangguan Nafas (Vesara Ardhe Gatera; Prof. Rizky Abdulah, Ph.D; Prof. Dr. Budi Setiabudiawan, dr., Sp.A(K)., M.Kes; Dr. Ida Musfiroh, M.Si)
Introduction: Respiratory distress syndrome is a disease caused by the condition
of premature babies and the inflammatory process in the lungs ...
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Code CallNo Lokasi Ketersediaan FFUP20220009 D018 Tersedia -
Perpustakaan Fakultas FarmasiJudul Seri -No. Panggil D018Penerbit Fakultas Farmasi Universitas Padjadjaran : Jatinangor., 2021 Deskripsi Fisik -Bahasa IndonesiaISBN/ISSN -Klasifikasi D018Tipe Isi -Tipe Media -Tipe Pembawa -Edisi -Subyek -Info Detil Spesifik -Pernyataan Tanggungjawab - -
Introduction: Respiratory distress syndrome is a disease caused by the condition
of premature babies and the inflammatory process in the lungs by the induction of
certain compounds. In this case, lipopolysaccharide is used as a compound from
the Escherichia coli bacteria group which can trigger an inflammatory response to
lung epithelial cells. In the condition of infants born prematurely, the management
of respiratory distress syndrome is done by administering corticosteroid therapy
and exogenous surfactant. However, the two treatments were deemed not optimal,
especially related to side effects and limited access. Therefore, other compounds
that are relatively effective and efficacy candidates are needed, one of which is
vitamin D. In previous studies, the potential of vitamin D as an anti-inflammatory
is related to its chemical structure, which is a natural secosteroid (steroid-like).
For optimization of clinical use, it is necessary to explore and confirm the role of
vitamin D, especially in the scope of the ability to maintain lung tissue or cells,
optimization of dose, the timing of administration, and mechanism of action as an
anti-inflammatory. Research Objectives: This research purposes to explored the
role of vitamin D in viability cells and to inhibits the inflammatory cytokines in
epithelial cell A549 with lipopolysaccharide-induced for the optimal doses and
windows therapy. The Research Stages That have been done: The first stage
carried out includes reviewing articles regarding the latest updates on vitamin D
research in the scope of the dose used, optimization of administration time, activity,
and mechanism of action. The study began by collecting studies/research in the
form of journals regarding vitamin D status on risk factors for respiratory distress
syndrome. Research journals related to the correlation of vitamin D with
respiratory distress syndrome were collected in the period 2009 – 2017 and
extracted according to the inclusion and exclusion criteria. The research continued
by exploring the ability of vitamin D, especially in defending lung epithelial cells
(A549) against lipopolysaccharide induction using the MTT Assay method with
variations in the test group and vitamin D-lipopolysaccharide concentration. The
vi
study was then continued with the observation of the ability of vitamin D to inhibit
the production of pro-inflammatory cytokines due to lipopolysaccharide induction.
The study was conducted using the Western Blot method with variations in the test
group and the concentration of vitamin D – Lipopolysaccharide. Results of
research that has been carried out: In review articles, the recommended dose to
the benefits of vitamin D supplementation ranges from 250 -1000 IU/kg in animals.
Then, further research and studies are needed regarding the benefits of vitamin D
supplementation therapy in humans and animals, especially in terms of the
molecular mechanism pathway. In addition to dose optimization, more complete
evidence is needed to determine the best vitamin D therapy, especially the
optimization of administration time, protein expression, and toxicity in humans and
animals. Therefore, the certainty of the recommended dose and optimization of the
timing of administration (pre-treatment or co-treatment) of vitamin D needs to be
studied more deeply as a strategy for treating pulmonary disorders before being
used clinically. In the cell viability test carried out, it was found that LPS induction
in A549 cells caused an increase in the activity of pro-inflammatory proteins
including nuclear factor nuclear factor kappa which is an activation of B cells (NFkB)
(55%, 57.9%), interleukin (IL)-1b. (45%, 29.4%), IL-6 (56.8%, 61.2%), IL-12
(44.4%, 81.8%), and tumor necrosis factor (TNF)-α (50.5%, 69.5%) at 6 and 12
hours compared to the control group. Testing the mechanism of action using the
Western blot method showed that LPS induction was able to increase the expression
of inflammatory cytokines such as NF- B, TNF-a, IL-1b, IL-6, and IL-12 with
regulated time (6 and 12 hours) and concentration. a relatively small amount of
vitamin D. The anti-inflammatory mechanism of vitamin D occurs through the
mechanism of reducing inflammatory cytokines such as NF-B, TNF-, IL-1ß, IL-6,
and IL-12, especially in the process of disrupting the NF-κB pathway. Conclusion:
We have successfully tested the ability of vitamin D with various doses and times of
administration in terms of maintaining the cell life cycle and inhibiting proinflammatory
cytokines as a study model to treat respiratory distress syndrome
through inhibition of the inflammatory pathway.
Keywords : Cytokines, Epithelial cell (A549), Inflammation, Lipopolysaccharide,
Vitamin D, Preterm birth, Respiratory distress syndrome. -
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