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人参皂苷 Rb1 对大鼠肠缺血再灌注肺损伤的保护作用。

Protective effect of ginsenoside Rb1 against lung injury induced by intestinal ischemia-reperfusion in rats.

机构信息

Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Jiefang Avenue, Wuhan 430030, Hubei, China.

出版信息

Molecules. 2013 Jan 17;18(1):1214-26. doi: 10.3390/molecules18011214.

DOI:10.3390/molecules18011214
PMID:23344209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6270255/
Abstract

Intestinal ischemia-reperfusion (I/R) is a critical event in the pathogenesis of multiple organ dysfunction syndromes (MODS). The lungs are some of the most vulnerable organs that are impacted by intestinal I/R. The aim of this study is to investigate whether ginsenoside Rb1 can ameliorate remote lung injury induced by intestinal I/R. Adult male Wistar rats were randomly divided into four groups: (1) a control, sham-operated group (sham group); (2) an intestinal I/R group subjected to 1 h intestinal ischemia and 2 h reperfusion (I/R group); (3) a group treated with 20 mg/kg ginsenoside Rb1 before reperfusion (Rb1-20 group); and (4) a group treated with 40 mg/kg ginsenoside Rb1 before reperfusion (Rb1-40 group). Intestinal and lung histology was observed. The malondialdehyde (MDA) levels in intestinal tissues were measured. Myeloperoxidase (MPO), TNF-α, MDA levels, wet/dry weight ratio and immunohistochemical expression of intracellular adhesion molecule-1 (ICAM-1) in lung tissues were assayed. In addition, a western blot of lung NF-kB was performed. Results indicated that intestinal I/R induced intestinal and lung injury, which was characterized by increase of MDA levels and pathological scores in intestinal tissues and MPO, TNF-α , MDA levels, wet/dry weight ratio and ICAM-1, NF-kB expression in the lung tissues. Ginsenoside Rb1 (20, 40 mg/kg) ameliorated intestinal and lung injury, decreased MPO, TNF-α, MDA levels, wet/dry weight ratio, ICAM-1 and NF-kB expression in lung tissues. In conclusion, ginsenoside Rb1 ameliorated the lung injuries by decreasing the NF-kB activation-induced inflammatory response.

摘要

肠缺血再灌注(I/R)是多器官功能障碍综合征(MODS)发病机制中的一个关键事件。肺部是受肠 I/R 影响最脆弱的器官之一。本研究旨在探讨人参皂苷 Rb1 是否可以改善肠 I/R 引起的远隔肺损伤。成年雄性 Wistar 大鼠随机分为四组:(1)对照组,假手术组(假手术组);(2)肠缺血 1 小时和再灌注 2 小时的肠 I/R 组(I/R 组);(3)再灌注前给予 20mg/kg 人参皂苷 Rb1 的组(Rb1-20 组);和(4)再灌注前给予 40mg/kg 人参皂苷 Rb1 的组(Rb1-40 组)。观察肠和肺组织学变化。测量肠组织丙二醛(MDA)水平。测定肺组织髓过氧化物酶(MPO)、TNF-α、MDA 水平、湿/干重比和细胞间黏附分子-1(ICAM-1)的免疫组织化学表达。此外,还进行了肺 NF-kB 的 Western blot。结果表明,肠 I/R 引起肠和肺损伤,其特征是肠组织 MDA 水平和病理评分升高,肺组织 MPO、TNF-α、MDA 水平、湿/干重比和 ICAM-1、NF-kB 表达增加。人参皂苷 Rb1(20、40mg/kg)改善了肠和肺损伤,降低了肺组织 MPO、TNF-α、MDA 水平、湿/干重比、ICAM-1 和 NF-kB 表达。结论:人参皂苷 Rb1 通过降低 NF-kB 激活诱导的炎症反应改善了肺损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/081d3d2b5c14/molecules-18-01214-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/4c6da5d0e31f/molecules-18-01214-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/58eea57b50fc/molecules-18-01214-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/9e7cf1d30c57/molecules-18-01214-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/c68d3efd1c05/molecules-18-01214-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/14d270a17094/molecules-18-01214-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/73512844219b/molecules-18-01214-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/08fc258d8fb3/molecules-18-01214-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/eac04acee6a0/molecules-18-01214-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/081d3d2b5c14/molecules-18-01214-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/4c6da5d0e31f/molecules-18-01214-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/58eea57b50fc/molecules-18-01214-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/9e7cf1d30c57/molecules-18-01214-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/c68d3efd1c05/molecules-18-01214-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/14d270a17094/molecules-18-01214-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/73512844219b/molecules-18-01214-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/08fc258d8fb3/molecules-18-01214-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/eac04acee6a0/molecules-18-01214-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b5a/6270255/081d3d2b5c14/molecules-18-01214-g009.jpg

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