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Published on: December 9, 2018
Gosha-Jinki-Gan Reduces Inflammation in Chronic Ischemic Stroke Mouse Models by Suppressing the Infiltration of
Mingli Xu1, Kaori Suyama2, Kenta Nagahori2
1Department of Immunoregulation, Institute of Medical Science, Tokyo Medical University, Tokyo 160-8402, Japan.
Insights
Gosha-jinki-gan (TJ107) effectively treats chronic ischemic stroke by reducing brain inflammation and infarct size. This oriental medicine offers a new therapeutic avenue for stroke recovery, improving neurological outcomes in mouse models.
Area of Science:
- Neuroscience
- Pharmacology
- Immunology
Background:
- Ischemic stroke is a leading cause of death and disability globally.
- Current treatments are mainly effective in the acute phase, leaving a gap in chronic stroke care.
- Chronic stroke involves persistent inflammation and tissue damage, worsening neurological deficits.
Purpose of the Study:
- To investigate the therapeutic potential of Gosha-jinki-gan (TJ107), an oriental medicine, for chronic ischemic stroke.
- To evaluate TJ107's effects on the intracerebral inflammatory response and neurological symptoms in a mouse model.
- To elucidate the mechanisms underlying TJ107's efficacy in chronic stroke.
Main Methods:
- Middle cerebral artery occlusion (MCAO) mouse model was used to induce ischemic stroke.
- Real-time RT-PCR was employed to examine the expression of inflammatory markers (F4/80, TLR2, TLR4, IL-23, IL-17, TNF-α, IL-1β) and GFAP.
- TJ107 was administered to MCAO mice to assess its therapeutic effects on infarct size and inflammation.
Main Results:
- MCAO mice exhibited increased expression of GFAP, F4/80, TLR2, TLR4, IL-1β, TNF-α, and IL-17 in chronic ischemic brain tissue.
- TJ107 administration significantly reduced infarct area and GFAP expression in MCAO mice.
- TJ107 suppressed macrophage infiltration and decreased the production of TNF-α, IL-1β, and IL-17.
Conclusions:
- This study demonstrates that TJ107 possesses therapeutic effects on chronic ischemic stroke.
- TJ107 mitigates the intracerebral inflammatory response associated with chronic stroke.
- Gosha-jinki-gan (TJ107) represents a promising therapeutic agent for improving outcomes in chronic ischemic stroke patients.
Abstract:
Ischemic stroke is a primary cause of cerebrovascular diseases and continues to be one of the leading causes of death and disability among patients worldwide. Pathological processes caused by vascular damage due to stroke occur in a time-dependent manner and are classified into three categories: acute, subacute, and chronic. Current treatments for ischemic stroke are limited to effectiveness in the early stages. In this study, we investigated the therapeutic effect of an oriental medicine, Gosha-jinki-gan (TJ107), on improving chronic ischemic stroke using the mouse model with middle cerebral artery occlusion (MCAO). The changes in the intracerebral inflammatory response (macrophages (F4/80), TLR2•4, IL-23, IL-17, TNF-α, and IL-1β) were examined using real-time RT-PCR. The MCAO mice showed the increased expression of glial fibrillary acidic protein (GFAP) and of F4/80, TLR2, TLR4, IL-1β, TNF-α, and IL-17 in the brain tissue from the MCAO region. This suggests that they contribute to the expansion of the ischemic stroke infarct area and to the worsening of the neurological symptoms of the MCAO mice in the chronic phase. On the other hand, the administration of TJ107 was proven to reduce the infarct area, with decreased GFAP expression, suppressed macrophage infiltration in the brain, and reduced TNF-α, IL-1β, and IL-17 production compared with the MCAO mice. This study first demonstrated Gosha-jinki-gan's therapeutic effects on the chronic ischemic stroke.

