마이크로웨이브를 조사한 흰쥐 폐조직의 Phospholipae A2 활성과 Arachidonic Acid Cascade계에 미치는 녹차 Catechin의 영향 (Effects of Green Tea Catechin on Microsomal Phospholipase A2 Activity and Arachidonic Acid Cascade in Rat Lung Exposed to Microwave)

서지정보

· 발행기관 : 한국식품영양과학회
· 수록지 정보 : 한국식품영양과학회지 / 41권 / 7호 / 936 ~ 942페이지
· 저자명 : 김미지

초록

In the present study, the effects of green tea catechin on microsomal phospholipase A2 (PLA2) activity and the arachidonic acid (AA) cascade in the lungs of microwave exposed rats were investigated. One Sprague- Dawley male rats weighting 100±10 g was randomly assigned to the normal group and three were assigned to the microwave exposed groups. The microwave exposed groups were subdivided into three groups according to the levels of dietary catechin supplementation: catechin free diet (MW) group, 0.25% catechin (MW-0.25C) group and 0.5% catechin (MW-0.5C) group. Rats were sacrificed on the 6th day after microwave irradiation (2.45 GHz, 15 min). The lung microsomal PLA2 activity in the MW and MW-0.25C groups was 30% and 15% greater than that of the normal group, respectively, whereas no significant difference between the normal group and MW-0.5C group was observed. The percentage of phosphatidylethanolamine (PE) hydrolyzed in the lung microsome in the MW, MW-0.25C and MW-0.5C group increased by 47%, 18% and 20%, respectively, due to microwave irradiation. The formation of thromboxane A2 (TXA2) in the lung microsome was 50% greater in the MW group than in the normal group. However, the levels of TXA2 in the MW-0.25C and MW-0.5C group were normal. The formation of prostacyclin (PGI2) in the lung microsome was 31% lower in the MW group than in the normal group, while the levels of PGI2 in the MW-0.25C and MW-0.5C group were similar to the normal group. The lung microsomal thiobarbituric acid reactive substances (TBARS) concentration, which can be used as an index of lipid peroxide was 34% greater in the MW group, when compared with the normal group. However, there was no difference between the MW-0.25C, MW-0.5C and normal groups. In conclusion, lung function appeared to be improved by green tea catechin supplementation due to its antithrombus action, which in turn controls the AA cascade system.

영어초록

In the present study, the effects of green tea catechin on microsomal phospholipase A2 (PLA2) activity and the arachidonic acid (AA) cascade in the lungs of microwave exposed rats were investigated. One Sprague- Dawley male rats weighting 100±10 g was randomly assigned to the normal group and three were assigned to the microwave exposed groups. The microwave exposed groups were subdivided into three groups according to the levels of dietary catechin supplementation: catechin free diet (MW) group, 0.25% catechin (MW-0.25C) group and 0.5% catechin (MW-0.5C) group. Rats were sacrificed on the 6th day after microwave irradiation (2.45 GHz, 15 min). The lung microsomal PLA2 activity in the MW and MW-0.25C groups was 30% and 15% greater than that of the normal group, respectively, whereas no significant difference between the normal group and MW-0.5C group was observed. The percentage of phosphatidylethanolamine (PE) hydrolyzed in the lung microsome in the MW, MW-0.25C and MW-0.5C group increased by 47%, 18% and 20%, respectively, due to microwave irradiation. The formation of thromboxane A2 (TXA2) in the lung microsome was 50% greater in the MW group than in the normal group. However, the levels of TXA2 in the MW-0.25C and MW-0.5C group were normal. The formation of prostacyclin (PGI2) in the lung microsome was 31% lower in the MW group than in the normal group, while the levels of PGI2 in the MW-0.25C and MW-0.5C group were similar to the normal group. The lung microsomal thiobarbituric acid reactive substances (TBARS) concentration, which can be used as an index of lipid peroxide was 34% greater in the MW group, when compared with the normal group. However, there was no difference between the MW-0.25C, MW-0.5C and normal groups. In conclusion, lung function appeared to be improved by green tea catechin supplementation due to its antithrombus action, which in turn controls the AA cascade system.

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