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- 저자 : 이우락 ( Woo Rak Lee ) (검색결과 2 건)
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급성 위염 동물 모델에서 감국(甘菊) 추출물과 아마인유(亞麻仁油) 혼합물의 위 점막 보호 효과
이진아 ( Jin A Lee ),김수현 ( Soo Hyun Kim ),김민주 ( Min Ju Kim ),안정현 ( Jeong-hyun Ahn ),박해진 ( Hae-jin Park ),이우락 ( Woo Rak Lee ),노성수 ( Seong-soo Roh ) 대한본초학회 2018 大韓本草學會誌 Vol.33 No.6
Objectives : The objective of this study was to investigate the protective effect of Flaxseed oil and Chrysanthemi Indici Flos 50% ethanol extract in an HCl/ethanol induced acute gastritis model. Methods : ICR mice were divided into 6 groups; normal mice (Nor), gastritic mice with distilled water (Veh), gastritic mice with 10 ㎎/㎏ sucralfate (SC), gastritic mice with 16 g/㎏ Flaxseed oil (FO), gastritic mice with FO + 50 ㎎/㎏ Chrysanthemi Indici Flos (FCL), and gastritic mice with FO + 100 ㎎/㎏ Chrysanthemi Indici Flos (FCH). Then, mice were orally administered with 150 mM HCl/60% ethanol and caused acute gastritis. After 1 hr, mice were sacrificed, and blood and stomach tissue were collected. Results : Administration of FCL and FCH to mice prior to the induction of gastritis was found to reduce gastric injury. reactive oxygen species (ROS) and peroxy nitrite (ONOO<sup>-</sup>) levels of stomach tissues were significantly decreased in FO, FCL, and FCH compared to Veh group. As results of stomach protein analyses, FCL and FCH effectively reduce inflammatory-related factors such as inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and interleukin 1 beta (IL-1β) in gastric lesion mice. In addition, nuclear factor kappa B p65 (NF-κB p65) and phosphorylation inhibitor of nuclear factor kappa Bα (p-IκBα) were down-regulated in FCL and FCH administrated gastric lesion mice. Conclusions : These results suggest that FCL and FCH has an inhibitory effect against gastric injury. Therefore, FCL and FCH has the potential to be used as a natural therapeutic drug.
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햄프씨드 오일이 고콜레스테롤식이를 급여한 흰쥐의 지질대사에 미치는 영향
이진아(Jin A Lee),노성수(Seong-Soo Roh),이우락(Woo Rak Lee),신미래(Mi-Rae Shin) 한국영양학회 2023 Journal of Nutrition and Health Vol.56 No.4
본 연구에서는 햄프씨드 오일이 고콜레스테롤혈증을 개선시키는 지 확인하기 위하여 Sprague-Dawley rat에 1.25% 콜레스테롤식이를 8주 동안 급여하였으며, 햄프씨드 오일을 두 농도 (저농도, 고농도)로 경구 투여한 후 혈액, 조직 분석을 통하여 지질개선 및 염증 완화 효과를 발휘하는지 분석하였다. 햄프씨드 오일 식이는AMPK/SREBP-2 경로를 경유하여 혈중콜레스테롤의 합성을 효과적으로 억제하였으며, PI3IK/Akt/NF-κB의 경로를 유의하게 억제하여 항염증 효과를 발휘함을 알 수 있었다. 이러한 신호전달의 경로는 간 조직에서 지질축적의 감소와도 관련이 있는 것으로 보인다. 이상의 결과를 종합해보면 햄프씨드 오일은 고콜레스테롤혈증의 예방 및 치료를 위한 잠재적 후보소재로서 가능성이 있음을 시사한다. Purpose: This study evaluates the potential protective effects of hemp (Cannabis sativa L.) seed oil supplementation in rats fed a high-cholesterol diet. Methods: Rats were fed a 1.25% cholesterol diet for 8 weeks, followed by oral administration of either of the two doses of hemp seed oil (HO) (0.5 mL/kg (HOL group) or 1 mL/kg (HOH group) body weight/day) or simvastatin at 10 mg/kg body weight/day. Oxidative stress, lipids, liver enzymes, and renal markers were measured in the serum. Western blot analysis was applied for evaluating the expressions of inflammatory makers. Results: Except for HDL-cholesterol, the altered levels of lipoproteins, aminotransferases, urea, and creatine kinases in hypercholesterolemic rats were significantly corrected by HO administration. Especially, compared to the HOH group, HOL treatment further reduced AST, ALT, creatinine, TC, and LDL-cholesterol levels. Moreover, both the atherogenic index and cardiac risk factor (CRF) in the HOL group were more restrained compared to the HOH group. Increased levels of p-AMPK coincided with the inhibition of SREBP-2 activation which subsequently suppressed the expression of HMGCR. Nuclear factor (NF)-κB activation coincided with the PI3K/Akt pathway activation and the increased phosphorylation of p38; these levels were significantly suppressed by HO treatment. In addition, HO treatment markedly reversed the changes in chemokines such as ICAM-1, VCAM-1, and MCP-1. Histological alterations induced by cholesterol overload in cardiac and hepatic tissues were ameliorated by HO supplementation. Conclusion: Taken together, our results indicate a low concentration of HO demonstrates improved dysfunctions caused by a high-cholesterol diet via inhibition of the PI3K/Akt/NF-κB signaling pathway.
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