Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibition

Tetramethylpyrazine (TMP) is an active component of the Chuanxiong, effectively crosses blood-brain barrier (BBB). It exhibits neuroprotective potential in cerebral ischemia-reperfusion injury (CIRI). This study performed middle cerebral artery occlusion/reperfusion (MCAO/R) surgery in rats to evalu...

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Main Authors: Yixin Zhang, Xin Zhang, Xiaocheng Shi, Weijing Liao, Junbin Lin
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-05-01
Series:Frontiers in Pharmacology
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Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2025.1594283/full
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author Yixin Zhang
Xin Zhang
Xiaocheng Shi
Weijing Liao
Junbin Lin
author_facet Yixin Zhang
Xin Zhang
Xiaocheng Shi
Weijing Liao
Junbin Lin
author_sort Yixin Zhang
collection DOAJ
description Tetramethylpyrazine (TMP) is an active component of the Chuanxiong, effectively crosses blood-brain barrier (BBB). It exhibits neuroprotective potential in cerebral ischemia-reperfusion injury (CIRI). This study performed middle cerebral artery occlusion/reperfusion (MCAO/R) surgery in rats to evaluate TMP’s efficacy and mechanisms in mitigating CIRI. Rats received intraperitoneal TMP (40 mg/kg) for 3 days prior to MCAO/R and continued for 14 days post-surgery. Behavioral tests were conducted using mNSS and Morris water maze tests. Histopathological analyses, including HE, Nissl, and TUNEL staining. mRNA sequencing revealed that RhoA and ROCK2 were upregulated in the CIRI model and downregulated by TMP treatment. GO enrichment and KEGG enrichment showed RhoA and ROCK were related to neuroplasticity. Western blot and immunofluorescence staining confirmed that TMP inhibited RhoA, ROCK2, phosphorylated LIMK, and phosphorylated cofilin expression. Additionally, TMP increased the levels of neuroplasticity-related proteins PSD95 and MAP2, promoting synaptic and dendritic regeneration. Administration of lysophosphatidic acid (LPA), a RhoA/ROCK pathway agonist, attenuated TMP’s neuroprotective effects, validating the pathway’s role in TMP-mediated protection. These findings indicate that TMP confers neuroprotection in CIRI by inhibiting the RhoA/ROCK pathway and enhancing neuroplasticity, underscoring its therapeutic potential in CIRI.
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spelling doaj-art-81a4bcd8428f420fb2eff54287da46002025-08-20T01:57:12ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-05-011610.3389/fphar.2025.15942831594283Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibitionYixin ZhangXin ZhangXiaocheng ShiWeijing LiaoJunbin LinTetramethylpyrazine (TMP) is an active component of the Chuanxiong, effectively crosses blood-brain barrier (BBB). It exhibits neuroprotective potential in cerebral ischemia-reperfusion injury (CIRI). This study performed middle cerebral artery occlusion/reperfusion (MCAO/R) surgery in rats to evaluate TMP’s efficacy and mechanisms in mitigating CIRI. Rats received intraperitoneal TMP (40 mg/kg) for 3 days prior to MCAO/R and continued for 14 days post-surgery. Behavioral tests were conducted using mNSS and Morris water maze tests. Histopathological analyses, including HE, Nissl, and TUNEL staining. mRNA sequencing revealed that RhoA and ROCK2 were upregulated in the CIRI model and downregulated by TMP treatment. GO enrichment and KEGG enrichment showed RhoA and ROCK were related to neuroplasticity. Western blot and immunofluorescence staining confirmed that TMP inhibited RhoA, ROCK2, phosphorylated LIMK, and phosphorylated cofilin expression. Additionally, TMP increased the levels of neuroplasticity-related proteins PSD95 and MAP2, promoting synaptic and dendritic regeneration. Administration of lysophosphatidic acid (LPA), a RhoA/ROCK pathway agonist, attenuated TMP’s neuroprotective effects, validating the pathway’s role in TMP-mediated protection. These findings indicate that TMP confers neuroprotection in CIRI by inhibiting the RhoA/ROCK pathway and enhancing neuroplasticity, underscoring its therapeutic potential in CIRI.https://www.frontiersin.org/articles/10.3389/fphar.2025.1594283/fulltetramethylpyrazinecerebral ischemia-reperfusion injuryneuroplasticityneuroprotectionnature products
spellingShingle Yixin Zhang
Xin Zhang
Xiaocheng Shi
Weijing Liao
Junbin Lin
Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibition
Frontiers in Pharmacology
tetramethylpyrazine
cerebral ischemia-reperfusion injury
neuroplasticity
neuroprotection
nature products
title Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibition
title_full Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibition
title_fullStr Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibition
title_full_unstemmed Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibition
title_short Tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia-reperfusion injury via RhoA/ROCK2 pathway inhibition
title_sort tetramethylpyrazine enhances neuroprotection and plasticity in cerebral ischemia reperfusion injury via rhoa rock2 pathway inhibition
topic tetramethylpyrazine
cerebral ischemia-reperfusion injury
neuroplasticity
neuroprotection
nature products
url https://www.frontiersin.org/articles/10.3389/fphar.2025.1594283/full
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