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微循环障碍及血必净在重症中暑中的保护作用。

Microcirculatory Disorders and Protective Role of Xuebijing in Severe Heat Stroke.

机构信息

Department of ICU, General Hospital of Guangzhou Military Command, Key Laboratory of Tropical Zone Trauma Care and Tissue Repair of PLA, Guangzhou, 510010, China.

The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510000, China.

出版信息

Sci Rep. 2018 Mar 14;8(1):4553. doi: 10.1038/s41598-018-22812-w.

DOI:10.1038/s41598-018-22812-w
PMID:29540802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5852149/
Abstract

This study was conducted to explore underlying mechanism of microcirculation dysfunction and protectiverole of Xuebijing in heat stroke. Forty rats were divided into: control, vehicle + heat stress (HS), superoxide dismutase (SOD) + HS, and Xuebijing + HS groups. Rats in heat stress groups were subjected to continuous heat stress in infant incubator 1 h after tail vein injection of the tested compound and spinotrapezius preparation. Velocity of blood flow through micro-vessels and vascular diameter were detected in real time. Another 27 rats were divided into: vehicle, SOD, and Xuebijing groups, then further divided into three subgroups each: control, Tcore = 38 °C, Tcore = 41 °C. Rats were sacrificed, and spinotrapezius single-cell suspensions were prepared for detecting SOD and reactive oxygen species (ROS). The results showed that heat stress decreased SOD activity, increased ROS levels, and reduced the blood flow rate. Xuebijing increased SOD activity, decreased ROS levels and exhibited a protective effect in terms of blood flow rate but was less protective than SOD. The survival time in Xuebijing + HS group was longer than that in vehicle group but shorter than that in SOD + HS group. The results suggested Xuebijing could decrease ROS levels and have protective effects in severe heat stroke.

摘要

本研究旨在探讨微循环功能障碍的潜在机制及血必净在中暑中的保护作用。将 40 只大鼠分为:对照组、 vehicle+HS 组、SOD+HS 组和 Xuebijing+HS 组。HS 组大鼠在尾静脉注射受试化合物和斜方肌制剂后 1 小时,置于婴儿培养箱中进行持续热应激。实时检测微血管血流速度和血管直径。另外 27 只大鼠分为:vehicle 组、SOD 组和 Xuebijing 组,每组再分为 3 个亚组:对照组、Tcore=38°C、Tcore=41°C。处死大鼠,制备斜方肌单细胞悬液,检测 SOD 和活性氧(ROS)。结果表明,热应激降低 SOD 活性,增加 ROS 水平,降低血流速度。血必净可增加 SOD 活性,降低 ROS 水平,并在血流速度方面具有保护作用,但不如 SOD 保护作用强。Xuebijing+HS 组的存活时间长于 vehicle 组,但短于 SOD+HS 组。结果提示血必净可降低 ROS 水平,对重症中暑具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/b0fa116ac8df/41598_2018_22812_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/7a0e942e1dca/41598_2018_22812_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/1af1ac629847/41598_2018_22812_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/821091a09025/41598_2018_22812_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/7633abc17554/41598_2018_22812_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/1ace366809c2/41598_2018_22812_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/803121d66ba8/41598_2018_22812_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/b0fa116ac8df/41598_2018_22812_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/7a0e942e1dca/41598_2018_22812_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/1af1ac629847/41598_2018_22812_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/821091a09025/41598_2018_22812_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/7633abc17554/41598_2018_22812_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/1ace366809c2/41598_2018_22812_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/803121d66ba8/41598_2018_22812_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8966/5852149/b0fa116ac8df/41598_2018_22812_Fig7_HTML.jpg

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Polydatin Alleviates Small Intestine Injury during Hemorrhagic Shock as a SIRT1 Activator.
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miR‑3613‑3p/MAP3K2/p38/caspase‑3 pathway regulates the heat‑stress‑induced apoptosis of endothelial cells.miR-3613-3p/MAP3K2/p38/caspase-3 通路调控内皮细胞热应激诱导的细胞凋亡。
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