Related Experiment Video
Updated: Dec 12, 2025
A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats
Published on: November 6, 2019
Tanshinone IIA Promotes Axonal Regeneration in Rats with Focal Cerebral Ischemia Through the Inhibition of
Jing Wang1, Guangxiao Ni2, Yanming Liu3
1Department of Chinese Medicine Diagnostics, Hebei University of Chinese Medicine, Shijiazhuang, Hebei 050200, People's Republic of China.
Purpose:
The aim of this study was to evaluate the neuroprotective effect of tanshinone IIA (TSA) on focal cerebral ischemia in rats and to investigate whether it was associated with Nogo-A/NgR1/RhoA/Rho-associated protein kinase 2 (ROCKII)/myosin light chain (MLC) signaling.
Methods:
In this study, focal cerebral ischemia animal model was used. Neurological deficit scores and infarction volume were investigated to evaluate the neuroprotection of TSA. Hematoxylin-eosin staining, Nissl staining, and immunofluorescence staining were conducted to detect ischemic changes in brain tissue and changes in neurofilament protein 200 (NF200) and growth-associated protein-43 (GAP-43) expression, respectively. Western blotting and qRT-PCR analyses were used to detect the expression levels of NF200, GAP-43 and Nogo-A/NgR1/RhoA/ROCKII/MLC pathway-related signaling molecules.
Results:
TSA treatment can improve the survival rate of rats, reduce the neurological score and infarct volume, and reduce neuron damage. In addition, TSA also increased axon length and enhanced expression of NF200 and GAP-43. Importantly, TSA significantly attenuated the expression of Nogo-A, NgR1, RhoA, ROCKII, and p-MLC, and thus inhibiting the activation of this signaling pathway.
Conclusion:
TSA promoted axonal regeneration by inhibiting the Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway, thereby exerting neuroprotective effects in cerebral ischemia rats, which provided support for the clinical application of TSA in stroke treatment.
Insights
Tanshinone IIA (TSA) demonstrated neuroprotective effects in rats with focal cerebral ischemia by promoting axonal regeneration. This action was linked to the inhibition of the Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Focal cerebral ischemia, a leading cause of stroke, results in significant neuronal damage and functional deficits.
- The Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway plays a critical role in inhibiting axonal regeneration after central nervous system injury.
Purpose of the Study:
- To evaluate the neuroprotective potential of tanshinone IIA (TSA) in a rat model of focal cerebral ischemia.
- To elucidate the underlying molecular mechanisms, specifically the involvement of the Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway.
Main Methods:
- Establishment of a focal cerebral ischemia animal model in rats.
- Assessment of neurological deficits, infarct volume, and histological changes (H&E, Nissl staining).
- Evaluation of neurofilament protein 200 (NF200) and growth-associated protein-43 (GAP-43) expression via immunofluorescence and Western blotting; analysis of Nogo-A/NgR1/RhoA/ROCKII/MLC pathway components using Western blotting and qRT-PCR.
Main Results:
- TSA treatment significantly improved survival rates, reduced neurological deficit scores, and decreased infarct volume.
- TSA administration enhanced axon length and upregulated the expression of NF200 and GAP-43.
- TSA markedly attenuated the expression of Nogo-A, NgR1, RhoA, ROCKII, and phosphorylated MLC (p-MLC), indicating inhibition of the pathway.
Conclusions:
- TSA exerts neuroprotective effects in focal cerebral ischemia by promoting axonal regeneration.
- The mechanism involves the inhibition of the Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway.
- These findings support the potential clinical application of TSA in stroke treatment.
