Related Experiment Video
Updated: May 8, 2026

Short-Duration Hypothermia Induction in Rats using Models for Studies examining Clinical Relevance and Mechanisms
Published on: March 3, 2021
Moderate hypothermia inhibits brain inflammation and attenuates stroke-induced immunodepression in rats
Li-Juan Gu1, Xiao-Xing Xiong, Takashi Ito
1Department of Neurosurgery, Stanford Stroke Center and Stanford Institute for Neuro-Innovation and Translational Neurosciences, Stanford University, Stanford, CA, USA; Department of Basic Medicine, Hangzhou Normal University, Hangzhou, China.
Aims:
Stroke causes both brain inflammation and immunodepression. Mild-to-moderate hypothermia is known to attenuate brain inflammation, but its role in stroke-induced immunodepression (SIID) of the peripheral immune system remains unknown. This study investigated the effects in rats of moderate intra-ischemic hypothermia on SIID and brain inflammation.
Methods:
Stroke was induced in rats by permanent distal middle cerebral artery occlusion combined with transient bilateral common carotid artery occlusion, while body temperature was reduced to 30°C. Real-time PCR, flow cytometry, in vitro T-cell proliferation assays, in vivo delayed-type hypersensitivity (DTH) reaction and confocal microscopy were used to study SIID and brain inflammation.
Results:
Brief intra-ischemic hypothermia helped maintain certain leukocytes in the peripheral blood and spleen and enhanced T-cell proliferation in vitro and delayed-type hypersensitivity in vivo, suggesting that hypothermia reduces SIID. In contrast, in the brain, brief intra-Ischemic hypothermia inhibited mRNA expression of anti-inflammatory cytokine IL-10 and proinflammatory mediators INF-γ, TNF-α, IL-2, IL-1β and MIP-2. Brief intra-Ischemic hypothermia also attenuated the infiltration of lymphocytes, neutrophils (MPO(+) cells) and macrophages (CD68(+) cells) into the ischemic brain, suggesting that hypothermia inhibited brain inflammation.
Conclusions:
Brief intra-ischemic hypothermia attenuated SIID and protected against acute brain inflammation.

