@article {1121, title = {High Dose Allicin with Vitamin C Improves EPCs Migration from the Patient with Coronary Artery Disease}, journal = {Pharmacognosy Journal}, volume = {12}, year = {2020}, month = {March 2020}, pages = {232-235}, type = {Original Article}, chapter = {232}, abstract = {

Endothelial Progenitor Cells (EPCs) have an important role in endothelial dysfunction repairment through neovasculogenesis and cardiac myocytes regeneration. However, EPCs migration is greatly reduced in the patient with Coronary Artery Disease (CAD). Allicin and Vitamin C are hypothesized to improve EPCs migration due to its antioxidant properties. Objective: To investigate the effect of Allicin and its combination with Vitamin C in EPCs migration of CAD patients. Material and Method: Mononuclear cells were isolated from CAD patients and cultured on fibronectin-coated plates with colony-forming unit Hill medium. The cells were divided into untreated (control), Allicin treatment (dose 100 mcg/ml, 200 mcg/ml, 400 mcg/ ml), and each dose of Allicin combined with 250 mcg/mL of Vitamin C. EPCs migration was assessed with Transwell Migration Assay Kit and evaluated by using statistical tests. Results: This research shows that EPC migration was significantly higher in the treatment. Allicin at all dose (dose 100 mcg/ml, 200 mcg/ml, 400 mcg/ml) and its combination with 250 mcg/mL of vitamin C compared to untreated group (p\<0.05). Allicin increase EPCs migration in a dosedependent manner. However, the only combination of 400 mcg/ml Allicin with 250 mcg/mL of vitamin C which has significantly higher EPCs migration compared to Allicin treatment alone. Conclusion: Allicin improves EPCs migration in a dose-dependent manner. Improvement of the migration only observed on the Allicin dose 400 mcg/ml with Vitamin C.

}, keywords = {Allicin, Antioxidant, Endothelial Progenitor, Migration}, doi = {10.5530/pj.2020.12.35}, author = {Yudi Her Oktaviono and Muhammad Rafdi Amadis and Makhyan Jibril Al-Farabi} } @article {1178, title = {Human Umbilical Cord Blood-derived Secretome Enhance Endothelial Progenitor Cells Migration on Hyperglycemic Conditions}, journal = {Pharmacognosy Journal}, volume = {12}, year = {2020}, month = {June 2020}, pages = {793-797}, type = {Original Article}, chapter = {793}, abstract = {

Hyperglycemia state is harmful to body{\textquoteright}s homeostasis. Uncontrolled hyperglycemic patients, especially patients with diabetes mellitus have a higher mortality risk of heart disease 2 to 4 times compared to non-hyperglycemic patients. Vascular endothelial impairment always been observed and found as a key feature of hyperglycemia state, which is correlated with reduced numbers and dysfunction of endothelial progenitor cells (EPCs). Objective: This paper aims to investigate the effect of hUCB-MSCs derived secretome treatment on the EPCs migration under hyperglycemia state. Materials and Methods: EPCs were isolated and cultured from peripheral blood samples and cultured for three days. Cultured EPCs were cultivated in 6-well plates until confluence and incubated with high glucose for 5 days, then placed in the modified Boyden chamber at the upper chamber with basal media. The lower chamber was supplemented with basal media and secretome at 2\%, 10\%, and 20\% concentration and VEGF treated group as a control. EPCS migration was evaluated using a Boyden chamber assay. Statistical analysis was performed using SPS 25.0. Results: EPCs migration were significantly higher when hUCB-MSCs-derived secretome was given in high glucose concentrations compared to the and control group (79.80 {\textpm} 5.07 vs 51.00 {\textpm} 5.15, p\<0.000). This study also showed that hUCB-MSCs-derived secretome increase EPCs migration under high glucose concentrations in a dose-dependent manner (p\<0.05). Conclusion: hUCB-MSCsderived secretome enhances EPCs migration under hyperglycemic state. This result may be of relevance for cell-free and regenerative therapeutic modality for a diabetic patient with coronary artery disease (CAD).

}, keywords = {Endothelial progenitor cells, Hyperglycemia state, Mesenchymal stem cells, Migration, Secretome}, doi = {10.5530/pj.2020.12.113}, author = {Yudi Her Oktaviono and Melly Susanti and Achmad Lefi and Ferry Sandra} }