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Neuroprotective effect of baicalin in a rat model of permanent focal cerebral ischemia
Xian-Kun Tu1, Wei-Zhong Yang, Song-Sheng Shi
1Department of Neurosurgery, The Affiliated Union Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Abstract:
This investigation was performed to determine the neuroprotective effect of baicalin on permanent cerebral ischemia injury in rats and the potential mechanisms in this process. Adult male Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (pMCAO). The rats were then received intraperitoneal injection with baicalin (10, 30 and 100 mg/kg) or vehicle. Morphological characteristic, neurological deficit scores, cerebral infarct volume and the enzymatic activity of myeloperoxidase (MPO) were measured 24 h after pMCAO. The mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were determined by RT-PCR. Neuronal apoptosis was determined by TUNEL staining and Western blot. Baicalin (30 and 100 mg/kg) reduced neurological deficit scores and cerebral infarct volume 24 h after pMCAO. Baicalin significantly decreased the enzymatic activity of MPO and the expression of iNOS mRNA and COX-2 mRNA in rat brain, it also significantly inhibited neuronal apoptosis and the expression of cleaved caspase-3 protein after pMCAO. Our results suggested that baicalin possesses potent anti-inflammatory and anti-apoptotic properties and attenuates cerebral ischemia injury. This protection might be associated with the downregulated expression of iNOS mRNA, COX-2 mRNA, and cleaved caspase-3 protein.
Insights
Baicalin demonstrates neuroprotective effects against cerebral ischemia injury in rats by reducing inflammation and neuronal apoptosis. This compound offers a potential therapeutic strategy for stroke by downregulating key inflammatory and apoptotic markers.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Cerebral ischemia injury, such as stroke, poses a significant health challenge.
- Identifying effective neuroprotective agents is crucial for mitigating stroke-related brain damage.
Purpose of the Study:
- To investigate the neuroprotective effects of baicalin on permanent cerebral ischemia injury in a rat model.
- To elucidate the underlying mechanisms, including anti-inflammatory and anti-apoptotic pathways.
Main Methods:
- Permanent middle cerebral artery occlusion (pMCAO) model in adult male Sprague-Dawley rats.
- Administration of baicalin (10, 30, 100 mg/kg) or vehicle via intraperitoneal injection.
- Assessment of neurological deficit, infarct volume, MPO activity, iNOS and COX-2 mRNA expression, and neuronal apoptosis (TUNEL, Western blot for cleaved caspase-3).
Main Results:
- Baicalin (30 and 100 mg/kg) significantly reduced neurological deficits and cerebral infarct volume 24 hours post-pMCAO.
- Baicalin treatment decreased myeloperoxidase activity, iNOS mRNA, and COX-2 mRNA expression in the brain.
- Baicalin inhibited neuronal apoptosis and cleaved caspase-3 protein expression.
Conclusions:
- Baicalin exhibits significant neuroprotective properties against permanent cerebral ischemia injury in rats.
- The protective effects are attributed to baicalin's anti-inflammatory and anti-apoptotic actions.
- Downregulation of iNOS, COX-2, and cleaved caspase-3 are key mechanisms mediating baicalin's therapeutic potential.
