Purpose of this study is to research the efficacy of Bee venom in Alzheimer΄s Disease mimic U87MG. Bee venom is consisted of melittin, apamin, MCD-peptide, Phospholipase A2, histamin, etc. To make Alzheimer΄s disease mimic cells, U87MG was incubated for 168 hours with 2.5 μM β-Amyloid. Changes ...
Purpose of this study is to research the efficacy of Bee venom in Alzheimer΄s Disease mimic U87MG. Bee venom is consisted of melittin, apamin, MCD-peptide, Phospholipase A2, histamin, etc. To make Alzheimer΄s disease mimic cells, U87MG was incubated for 168 hours with 2.5 μM β-Amyloid. Changes in morphology were confirmed by microscopy, and peptides inside the cell were measured under staining-free conditions using homo-tomography. SRB analysis was performed to analyze cell viability. qPCR analysis was conducted to analyze mRNA expression levels of pro-inflammatory cytokine(NF-κB, COX-2, TNF-α, IL-1). Western blot was performed to measure the expression level of Caspase 3. Bee venom was not cytotoxic at concentrations below 10 ㎍/㎖. The study was conducted at the maximum concentration without cytotoxicity. Microscopy confirmed changes in cell morphology, and Bee venom reduced β-Amyloid accumulation in homo-tomography. In Bee venom treatment, mRNA expression level was not decreased in NF-κB and was decreased in COX-2, TNF-α and IL-1. As a result of western blot, the expression level of Caspase 3 decreased in bee venom treated group. The results suggest that Bee venom has an effect of inhibiting apoptosis in Alzheimer΄s disease mimic U87MG, inhibiting inflammatory responses, and preventing apoptosis. In addition, it prevented cell accumulation of β-Amyloid, an important pathogen in Alzheimer΄s disease, and confirmed the possibility of the effect of Bee venom on Alzheimer΄s disease treatment.
Purpose of this study is to research the efficacy of Bee venom in Alzheimer΄s Disease mimic U87MG. Bee venom is consisted of melittin, apamin, MCD-peptide, Phospholipase A2, histamin, etc. To make Alzheimer΄s disease mimic cells, U87MG was incubated for 168 hours with 2.5 μM β-Amyloid. Changes in morphology were confirmed by microscopy, and peptides inside the cell were measured under staining-free conditions using homo-tomography. SRB analysis was performed to analyze cell viability. qPCR analysis was conducted to analyze mRNA expression levels of pro-inflammatory cytokine(NF-κB, COX-2, TNF-α, IL-1). Western blot was performed to measure the expression level of Caspase 3. Bee venom was not cytotoxic at concentrations below 10 ㎍/㎖. The study was conducted at the maximum concentration without cytotoxicity. Microscopy confirmed changes in cell morphology, and Bee venom reduced β-Amyloid accumulation in homo-tomography. In Bee venom treatment, mRNA expression level was not decreased in NF-κB and was decreased in COX-2, TNF-α and IL-1. As a result of western blot, the expression level of Caspase 3 decreased in bee venom treated group. The results suggest that Bee venom has an effect of inhibiting apoptosis in Alzheimer΄s disease mimic U87MG, inhibiting inflammatory responses, and preventing apoptosis. In addition, it prevented cell accumulation of β-Amyloid, an important pathogen in Alzheimer΄s disease, and confirmed the possibility of the effect of Bee venom on Alzheimer΄s disease treatment.
※ AI-Helper는 부적절한 답변을 할 수 있습니다.