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Updated: Feb 28, 2026
A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats
Published on: November 6, 2019
[Minocycline Prevent Microglial Activation via Suppression of Adenosine A 2A Receptor in a Rat Stroke
Tao Tao1, Jie Fu1, Yong-Gang Liu1
1Department of Neurology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Objectives:
To investigate whether minocycline could inhibit neuroinflammation induced by microglia activation through suppression of adenosine A2Areceptor (Aexpression in rats after cerebral ischemia/reperfusion (I/R) injury.
Methods:
Thirty male Sprageue-Dawley rats were randomly divided into 3 groups: sham group, I/R group and minocycline group. The rats were subjected to occlusion of the right middle cerebral artery (MCAO) for 2 h to establish stroke I/R model, and 3 mg/kg minocycline was injected intravenously immediately after reperfusion twice a day in minocycline group. At 24 h after I/R, the inflammatory cytokines IL-1β and IL-6 in peri-infarct region were measured by Western blot, microglia activation was detected by double-immunofluorescence labeling. A2AR density was detected by immunohistofluorescence and Western blot.
Results:
The number of CD11b-positive cells in I/R group was increased when compared with that in sham group. The expressions of IL-1β, IL-6 and A2AR were markedly up-regulated after I/R. Minocycline significantly decreased the expressions of IL-1β, IL-6 and A2AR and the number of CD11b-positive cells in peri-infarct region.
Conclusion:
Minocycline could prevent cerebral ischemia induced neuroinflammation by the suppression of microglial activation, which may be related to down-regulation of A2AR expression.
Insights
Minocycline treatment reduced neuroinflammation and microglial activation following stroke in rats. This effect may be linked to the suppression of adenosine A2A receptor expression after cerebral ischemia.
Area of Science:
- Neuroscience
- Pharmacology
- Pathology
Background:
- Cerebral ischemia/reperfusion (I/R) injury triggers neuroinflammation via microglia activation.
- Adenosine A2A receptors (A2AR) play a role in modulating inflammatory responses in the brain.
Purpose of the Study:
- To determine if minocycline inhibits neuroinflammation by suppressing A2AR expression in a rat model of cerebral I/R injury.
- Investigate the impact of minocycline on microglia activation and inflammatory cytokine levels post-stroke.
Main Methods:
- A rat model of middle cerebral artery occlusion (MCAO) was used to induce I/R injury.
- Minocycline was administered intravenously post-reperfusion.
- Levels of IL-1β, IL-6, A2AR expression, and microglia activation (CD11b-positive cells) were assessed in the peri-infarct region.
Main Results:
- I/R injury significantly increased CD11b-positive cells, IL-1β, IL-6, and A2AR expression compared to sham controls.
- Minocycline treatment markedly reduced these markers of neuroinflammation and microglia activation.
- Minocycline administration led to a significant decrease in A2AR density and expression.
Conclusions:
- Minocycline effectively mitigates neuroinflammation and microglial activation after cerebral I/R injury.
- The neuroprotective effects of minocycline may involve the down-regulation of adenosine A2A receptor expression.
- This study suggests minocycline as a potential therapeutic agent for stroke by targeting neuroinflammation.
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