Potensi Sinamaldehid sebagai Anti Hiperpigmentasi secara In Silico

Permasalahan kulit yang sering ditemui yaitu hiperpigmentasi yang terjadi akibat adanya sintesis melanin berlebihan yang menyebabkan penggelapan warna kulit. Hiperpigmentasi dapat diatasi dengan agen anti hiperpigmentasi yang beraktivitas dalam menghambat proses sintesis melanin. Sintesis melanin dapat dihambat dengan berbagai cara salah satunya dengan menghambat aktivitas tyrosinase. Tyrosinase merupakan enzim yang berperan dalam mengkatalisis proses biosintesis melanin. Sinamaldehid merupakan senyawa bahan alam banyak ditemukan pada tanaman Cinnamomum burmanni mempunyai aktivitas sebagai antioksidan. Penelitian ini bertujuan untuk mengetahui potensi sinamaldehid dalam menghambat tyrosinase yang akan dibandingkan dengan native liganya secara in silico. Uji in silico dilakukan secara docking molecular dengan tahapan yaitu preparasi dan optimasi sinamaldehid, preparasi tyrosinase serta validasi dan docking. Metode docking molecular telah dinyatakan valid karena RMSD (root mean square distance) yang diperoleh tidak lebih dari 3 Å. Analisis data dilakukan dengan melihat energi ikatan yang dihasilkan dan ikatan yang terbentuk antara senyawa dengan residu asam amino pada protein. Nilai energi ikatan yang diperoleh antara ikatan sinamaldehid dengan tyrosinase adalah-6,21 kkal/mol. Sedangkan energi ikatan antara tyrosinase dengan native ligandnya -4,79 kkal/mol. Hal tersebut menunjukkan afinitas dari sinamaldehid pada protein tyrosinase lebih besar dibandingkan native ligandnya, sehingga sinamaldehid dikatakan memiliki potensi sebagai anti hiperpigmentasi dengan mekanisme molecular berupa inhibitor protein target tyrosinase sehingga dapat menghambat aktivitas enzim tyrosinase.

Sudden unexpected death due to hereditary angioedema — A case report

Angioedema related to deficiency of the C1- esterase inhibitor protein (C1-inh) is characterized by lack of response to therapies, which include antihistamines, steroids and epinephrine. In case of laryngeal edema, mortality rate is an estimated mammoth 30 percent. The first case of such acquired form of angioedema related to the deficiency in C1- esterase inhibitor was published in 1972. In the present case, we entail details of one such case.,

Phosphatidylethanolamine binding protein 1 enhances sensitivity of gastric cancer cell to 5-fluorouracil via inhibition of cell proliferation, migration and invasion

Purpose: To determine the association between phosphatidylethanolamine binding protein 1, which is an Raf kinase inhibitor protein (RKIP), and 5-fluorouracil (5-FU) via analysis of the association between RKIP and clinical responses in individuals treated using fluorouracil-based chemotherapy.Methods: Human gastric cancer cell lines MGC-803 and SGC-7901 were used in this study. Cell viability was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis and migration were determined with flow cytometry and Transwell chamber assays, respectively. The mRNA and protein expressions of apoptosis-related factors were assayed using realtime polymerase chain reaction (RT-PCR) and Western blotting, respectively, while the expression of RKIP was determined by immunohistochemical staining.Results: Chemotherapeutic drug (5-FU) treatment induced low RKIP expression levels in tumorigenic GC cells, thereby sensitizing the cells to apoptosis (8.57 vs 1.25 %, p < 0.01). The highest RKIP level correlated well with initiation of apoptosis (4.20 vs 1.25 %, p < 0.01). Following in vitro downregulation of RKIP, there was increase in the viability and proliferation of RKIP-inhibited cells over time, and these changes were linked to alterations in cell cycle phases and increased optical density in MTT proliferation assay (1.55 vs 1.18, p < 0.01). In vitro Transwell assay measurement revealed an association between RKIP downregulation and enhancement of cell migration potential (652 vs 436, p < 0.01). Ectopic RKIP expression restored the apoptotic sensitivity of resistant cells (14.30 vs 1.36 %, p <0.01). This sensitization was annulled by upregulation of survival routes. Reduction of RKIP by expression of antisense and siRNA conferred resistance on cancer cells sensitive to 5-FU-mediated apoptosis (6.88 vs 2.13 %, p < 0.01).Conclusion: Thus, RKIP is a promising therapeutic strategy for improving the efficacy of clinically relevant chemotherapeutic drugs for GC. Keywords: Gastric cancer, Raf kinase inhibitor protein, Cell proliferation, Invasion, Apoptosis, Chemotherapy, Phosphatidylethanolamine binding protein 1