Pretreatment with baicalin attenuates hypoxia and glucose deprivation-induced injury in SH-SY5Y cells / 中国结合医学杂志

<p><b>OBJECTIVE</b>To explore the neuroprotective effects of baicalin against hypoxia and glucose deprivation-reperfusion (OGD/RO)-induced injury in SH-SY5Y cells.</p><p><b>METHODS</b>SH-SY5Y cells were divided into a control group, a OGD/RO group, which was subject to OGD/RO induction; and 3 baicalin groups subject to baicalin (1, 5, 25 μmol/L) for 2 h before induction of OGD/RO (low-, medium-, and high-dose baicalin groups). Cell viability was detected by thiazolyl blue tetrazolium bromide (MTT) assay and flow cytometric analysis was used to detect cell apoptosis. Real-time polymerase chain reaction was performed to determine the mRNA expression of caspase-3 gene. Western blot analysis was conducted to determine the expression of nuclear factor (NF)-κB and N-methyl-daspartic acid receptor-1 (NMDAR1).</p><p><b>RESULTS</b>Baicalin could significantly attenuate OGD/RO mediated apoptotic cell death in SH-SY5Y cells; the apoptosis rates in the low-, medium- and high-dose groups were 12.1%, 7.9%, and 5.4%, respectively. Western blot and real-time PCR analysis revealed that significant decrease in caspase-3 expression in the baicalin group compared with the OGD/RO group (P<0.01). Additionally, down-regulation of NF-κB and NMDAR1 was observed in the baicalin group compared with those obtained from the OGD/RO group. Compared with the low-dose baicalin group, remarkable decrease was noted in the medium- and high-dose groups (P<0.01).</p><p><b>CONCLUSION</b>Baicalin pre-treatment attenuates brain ischemia reperfusion injury by suppressing cellular apoptosis.</p>

Baicalin attenuates focal cerebral ischemic reperfusion injury by inhibition of protease-activated receptor-1 and apoptosis / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the neuro-protective effects of baicalin in Wistar rats with focal cerebral ischemic reperfusion injury.</p><p><b>METHODS</b>Ninety adult male Wistar rats weighing 320-350 g were randomly divided into the following groups (n=5): (a) sham control group; (b) vehicle group, subjected to middle cerebral artery occlusion and received vehicle intraperitoneally; (c-e) baicalin groups, which were subjected to the middle cerebral artery occlusion and treated with baicalin 25, 50 and 100 mg/kg, respectively. The neurological scores were determined at postoperative 1, 3 and 7 d after the treatment. The expression of protease-activated receptor-1 (PAR-1), PAR-1 mRNA and Caspase-3 were determined using Western blot, reverse transcription polymerase chain reaction (RTPCR) analysis and immunohistochemistry, respectively.</p><p><b>RESULTS</b>Significant decrease was noted in the neurological score in the baicalin group compared with that of the vehicle group (P<0.01). Additionally, down-regulation of PAR-1 mRNA, PAR-1 and Caspase-3 was observed in the baicalin groups compared with those obtained from the vehicle group (P<0.01). Compared with the low-dose baicalin group (25 mg/kg), remarkable decrease was noted in neurological score, and the expression of PAR-1 mRNA, PAR-1 as well as Caspase-3 in the high-dose group (P<0.05).</p><p><b>CONCLUSION</b>Baicalin showed neuro-protective effects in focal cerebral ischemic reperfusion injury through inhibiting the expression of PAR-1 and apoptosis.</p>

Effect of baicalin on protease-activated receptor-1 expression and cell apoptosis in brain of rat with intracerebral hemorrhage / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate the protective effect and mechanism of baicalin on nerve tissue in rat with intracerebral hemorrhage (ICH).</p><p><b>METHODS</b>Rats were randomly divided into five groups: the sham-operated group, the ICH model group, and the three baicalin treated groups treated respectively with small, medium and large doses of baicalin. ICH rat model was established by injecting collagenase VII into caudate nucleus. Baicalin was given by peritoneal injection to the baicalin treated groups, and saline was given to the other two groups once a day started from 2 h after modeling. Animals were sacrificed in batches on the 1st, 3rd, 5th and 10th day of treatment to take their brains for detecting protease-activated receptor-1 (PAR-1) expression and cell apoptosis in brain tissue surrounding hematoma by Western blot and TUNEL method, respectively. And the water content of brain was estimated by dry-wet weight method.</p><p><b>RESULTS</b>Compared with the model group, the PAR-1 expression and TUNEL-positive cells were significantly reduced in the baicalin treated groups; and brain edema was also significantly reduced (P<0.01).</p><p><b>CONCLUSIONS</b>The up-regulated PAR-1 expression after ICH in rats might play an important role in inducing cell apoptosis and brain edema. Baicalin shows significant protective effect on ICH rats, which may be related to its effects in inhibiting PAR-1 expression and decreasing apoptosis cells, so as to reduce brain edema.</p>

Protective effect of Noningkang Granule on brain in intracerebral hemorrhagic rats / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate the protective effect and mechanism of Naoningkang Granule (NG), a Chinese medicinal preparation formulated for clearing heat and detoxication, on brain tissue in intracerebral hemorrhagic (ICH) rats.</p><p><b>METHODS</b>Rats were randomly divided into 5 groups: the sham operated group, the model group and the high-, medium- and low-dose NG groups. Collagenase VII was injected into caudate nucleus to induce rat model of ICH, corresponding dosage of NG was started to give to the 3 NG groups by gastrogavage 2 h after modeling, and saline of equal volume was given to the other 2 groups instead. The brain tissue of rats was taken in batches at the 3rd and 7th day for pathomorphological observation using HE stain, and detection of thrombin receptor-1 (PAR-1) expression and nerve cell apoptosis in the peripheral tissue of hemorrhagic brain with immunohistochemistry and TUNEL assay, as well as for measurement of water content in brain tissue by wet-to-dry weight method.</p><p><b>RESULTS</b>PAR-1 expression elevated in the model rats. As compared with the model group, the pathomorphological changes significantly improved, PAR-1 expression decreased, apoptotic cells re-duced and brain edema alleviated in the 3 NG groups.</p><p><b>CONCLUSION</b>Overexpression of PAR-1 in the brain tissue might mediate the nerve cell apoptosis and brain edema in ICH rats. The mechanism of NG in protecting hemor-rhagic brain tissue might be related with its actions in inhibiting the post-cerebral high PAR-1 expression to re-duce cell apoptosis and relieve brain edema.</p>