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Abstrak :
Glutamat adalah molekul monoamin yang mengatur sel-sel saraf. Senyawa ini juga memiliki reseptor pada sel imun. Regulasi glutamat sel imun termasuk kemotaksis, diferensiasi, proliferasi dan apoptosis. Tujuan dari penelitian ini adalah menentukan produksi sitokin PBMC yang dirangsang dengan glutamat. Sitokin dinilai dengan metode elisa. PBMC dikumpulkan dari 10 donor pria sehat. PBMC 7x105 yang diisolasi dirangsang dengan glutamat atau tidak diobati, diinkubasi selama 24 jam 5% CO2 37 oC dalam media lengkap asam amino, vitamin B kompleks dan ion. Terjadi penurunan sitokin pada kelompok yang distimulasi glutamat daripada kelompok kontrol. Dijelaskan bahwa glutamat berubah menjadi metabolit dalam mitokondria. Sebagai kesimpulan, hasil ini menunjukkan bahwa glutamat memiliki dampak menurunkan produksi sitokin pada PBMC manusia yang sehat. ......Glutamate are monoamine molecules that regulate nerve cells. These compounds also have receptors on immune cells. Glutamate regulation of immune cells include chemotaxis, differentiation, proliferation and apoptosis. Aim of this study is determining cytokine production PBMC stimulated with glutamate. Cytokine was assessed by elisa method. PBMC was collected from 10 healthy male donors. Isolated 7x105 PBMCs were stimulated with Glutamate or untreated, incubated for 24 hours 5 % CO2 37 oC in a complete medium of amino acids, vitamin B complex and ions. A decrease in cytokine in glutamate treated group than control group. It was suggested that Glutamate role as metabolite in mitochondria. As conclusion, these results suggest that glutamate have suppresing impact on cytokine production in healthy human PBMC.

Abstrak :
Inflamasi memiliki peran penting dalam perkembangan berbagai kondisi patologis, yang dimediasi oleh aktivasi berbagai jalur pensinyalan, termasuk jalur IKK-NF-κB. Silybin, senyawa flavonolignan yang ditemukan dalam Milk Tistle (Silybum marianum L) telah digunakan secara tradisional untuk mengobati penyakit hati dan telah dilaporkan memiliki aktivitas anti-inflamasi, antifibrotik, dan imunomodulator. Namun, mekanisme molekuler silybin sebagai agen antiinflamasi potensial terhadap jalur pensinyalan IKKNF- κB masih belum jelas. Penelitian ini menggunakan simulasi penambatan molekuler menggunakan Autodock 4.0 untuk menyelidiki interaksi antara Silybin dan NF-κB. Hasil penelitian menunjukkan bahwa silybin menunjukkan inhibisi kompetitif-ATP dan memiliki afinitas pengikatan yang tinggi untuk makromolekul IkB kinase beta (IKKβ) dan NIK (NF-kB-inducing kinase), dengan energi pengikatan -9,73 kkal/mol pada rantai A dan -9,84 kkal/mol pada rantai B IkB kinase beta (IKKβ) serta -9,34 kkal/mol pada makromolekul NIK (NF-kB-inducing kinase). Konstanta Inhibisi (Ki) ditemukan masingmasing 74,14 nM pada rantai A dan 61,12 nM pada rantai B IkB kinase beta (IKKβ) serta 141,81 nM mol pada NIK (NF-kB-inducing kinase). Temuan ini menunjukkan bahwa silybin memiliki potensi untuk menghambat jalur pensinyalan IKK-NF-κB, sehingga memberikan efek anti-inflamasi. Selain itu, silybin menunjukkan afinitas pengikatan yang lebih tinggi jalur persinyalan kanonikal dibanding jalur perisnyalan alternatif. Studi ini memberikan wawasan tentang mekanisme molekuler silybin sebagai agen antiinflamasi potensial dan aplikasi terapeutiknya dalam terapi penyakit yang berhubungan dengan Inflamasi. ......Inflammation has a crucial role in the progression of various pathological conditions, mediated by the activation of multiple signaling pathways, including the IKK-NF-κB pathway. Silybin, a flavonolignan compound extracted from Milk thistle (Silybum marianum L.) has been traditionally used to treat liver disorders and exhibits pharmacological properties, including anti-inflammatory, antifibrotic, and immunomodulatory activities. However, the molecular mechanisms underlying Silybin's anti-inflammatory potential, particularly its interaction with the IKK-NF-κB signaling pathway, remain unclear. This study employed molecular docking simulations using Autodock 4.0 to investigate the interaction between Silybin and NF-κB. The results showed that silybin exhibited competitive-ATP inhibition and high binding affinity for IkB kinase beta (IKKβ) and NIK (NF-kB-inducing kinase) macormolecule, with binding energies of -9.73 kcal/mol on the A chain and -9.84 kcal/mol on the B chain of IkB kinase beta (IKKβ) and -9.34 kcal/mol on NIK (NF-kB-inducing kinase). Inhibition constants (Ki) were found to be 74.14 nM on chain A and 61.12 nM on chain B of IkB kinase beta (IKKβ) and 141.81 nM mol on NIK (NF-kB-inducing kinase), respectively. Notably, silybin displays higher binding affinity for the canonical pathway compared to the alternative pathway. These findings suggest that silybin has the potential to inhibit IKKNF- κB signaling, leading to anti-inflammatory effects. This study provides valuable insights into the molecular mechanism of silybin as a potential anti-inflammatory agent and its therapeutic applications in inflammation-related diseases.

Abstrak :
ABSTRACT
The immune system, inflammation and hypertension are related to each other. Innate and adaptive immunity system triggers an inflammatory process, in which blood pressure may increase, stimulating organ damage. Cells in innate immune system produce ROS, such as superoxide and hydrogen peroxide, which aimed at killing pathogens. Long-term inflammation process increases ROS production, causing oxidative stress which leads to endothelial dysfunction. Endothelial function is to regulate blood vessel tone and structure. When inflammation lasts, NO bioavailability decreases, disrupting its main function as vasodilator, so that blood vessels relaxation and vasodilatation are absent. Effector T cells and regulatory lymphocytes, part of the adaptive immune system, plays role in blood vessels constriction in hypertension. Signals from central nervous system and APC activates effector T lymphocyte differentiation and accelerate through Th-1 and Th-17 phenotypes. Th-1 and Th-17 effectors participate in inflammation which leads to increased blood pressure. One part of CD4+ is the regulatory T cells (Tregs) that suppress immune response activation as they produce immunosuppressive cytokines, such as TGF-I and IL-10. Adoptive transfer of Tregs cells can reduce oxidative stress in blood vessels, endothelial dysfunction, infiltration of aortic macrophages and T cells as well as proinflammatory cytokine levels in plasma circulation.