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Effect of baicalin on hippocampal damage in kainic acid-induced epileptic mice

View Article: PubMed Central - PubMed

ABSTRACT

The aim of the present study was to determine the effect of baicalin on the expression of miR-497 and its target B-cell lymphoma-2 (Bcl-2) in the hippocampus of kainic acid (KA)-induced epileptic mice. To establish status epilepticus (SE), 0.1 µg/5 µl KA was injected into the lateral cerebral ventricle in mice, which then received an intraperitoneal injection of baicalin (100 mg/kg) after 1 and 8 h. Hematoxylin and eosin staining was used to observe the pathological changes in morphology and neuronal apoptosis was determined by terminal transferase-mediated dUTP nick end-labeling staining. Western blot analysis was used to detect the expression of Bcl-2 and cleaved caspase-3 proteins in the hippocampus, while reverse transcription-quantitative polymerase chain reaction was used to quantify hippocampal miR-497 expression. The results showed that baicalin significantly attenuated neuronal damage and apoptosis in the hippocampus 72 h after SE. In addition, baicalin decreased SE-induced expression of miR-497 and cleaved caspase-3 protein, while upregulating the expression of Bcl-2 protein. In conclusion, the present results suggest that baicalin possesses potent antiapoptotic properties and attenuates hippocampal injury in mice after SE, which may be associated with the downregulation of miR-497 and cleaved caspase-3 and the upregulation of Bcl-2.

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Protein expression of cleaved caspase-3 and Bcl-2 in the hippocampus. Effects of baicalin on the protein levels of (A) caspase-3 and (B) Bcl-2 at 72 h after SE as evidenced by western blots. Data are expressed as the ratio the respective proteins to β-actin internal control and are represented as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. Bcl-2, B-cell lymphoma; SE, status epilepticus.
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f3-etm-0-0-3461: Protein expression of cleaved caspase-3 and Bcl-2 in the hippocampus. Effects of baicalin on the protein levels of (A) caspase-3 and (B) Bcl-2 at 72 h after SE as evidenced by western blots. Data are expressed as the ratio the respective proteins to β-actin internal control and are represented as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. Bcl-2, B-cell lymphoma; SE, status epilepticus.

Mentions: The levels of cleaved caspase-3 and Bcl-2 (relative to β-actin) in brain tissue removed from mice sacrificed 72 h following the induction of SE was analyzed using western blotting. The results showed that SE increased cleaved caspase-3 protein expression, which was suppressed by baicalin (Fig. 3A) (P<0.05). By contrast, SE upregulated antiapoptotic Bcl-2 protein expression (SE, 0.42±0.07 vs. sham, 0.21±0.03; P<0.001) (Fig. 3B). Baicalin treatment resulted in greater increases in Bcl-2 expression as a result of SE compared with SE alone (baicalin, 0.55±0.08 vs. SE, 0.42±0.07; P=0.003) (Fig. 3B). These results suggest that baicalin administration following KA-induced SE leads to lower expression of proteins associated with neuronal apoptosis in the hippocampus.


Effect of baicalin on hippocampal damage in kainic acid-induced epileptic mice
Protein expression of cleaved caspase-3 and Bcl-2 in the hippocampus. Effects of baicalin on the protein levels of (A) caspase-3 and (B) Bcl-2 at 72 h after SE as evidenced by western blots. Data are expressed as the ratio the respective proteins to β-actin internal control and are represented as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. Bcl-2, B-cell lymphoma; SE, status epilepticus.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998122&req=5

f3-etm-0-0-3461: Protein expression of cleaved caspase-3 and Bcl-2 in the hippocampus. Effects of baicalin on the protein levels of (A) caspase-3 and (B) Bcl-2 at 72 h after SE as evidenced by western blots. Data are expressed as the ratio the respective proteins to β-actin internal control and are represented as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. Bcl-2, B-cell lymphoma; SE, status epilepticus.
Mentions: The levels of cleaved caspase-3 and Bcl-2 (relative to β-actin) in brain tissue removed from mice sacrificed 72 h following the induction of SE was analyzed using western blotting. The results showed that SE increased cleaved caspase-3 protein expression, which was suppressed by baicalin (Fig. 3A) (P<0.05). By contrast, SE upregulated antiapoptotic Bcl-2 protein expression (SE, 0.42±0.07 vs. sham, 0.21±0.03; P<0.001) (Fig. 3B). Baicalin treatment resulted in greater increases in Bcl-2 expression as a result of SE compared with SE alone (baicalin, 0.55±0.08 vs. SE, 0.42±0.07; P=0.003) (Fig. 3B). These results suggest that baicalin administration following KA-induced SE leads to lower expression of proteins associated with neuronal apoptosis in the hippocampus.

View Article: PubMed Central - PubMed

ABSTRACT

The aim of the present study was to determine the effect of baicalin on the expression of miR-497 and its target B-cell lymphoma-2 (Bcl-2) in the hippocampus of kainic acid (KA)-induced epileptic mice. To establish status epilepticus (SE), 0.1 &micro;g/5 &micro;l KA was injected into the lateral cerebral ventricle in mice, which then received an intraperitoneal injection of baicalin (100 mg/kg) after 1 and 8 h. Hematoxylin and eosin staining was used to observe the pathological changes in morphology and neuronal apoptosis was determined by terminal transferase-mediated dUTP nick end-labeling staining. Western blot analysis was used to detect the expression of Bcl-2 and cleaved caspase-3 proteins in the hippocampus, while reverse transcription-quantitative polymerase chain reaction was used to quantify hippocampal miR-497 expression. The results showed that baicalin significantly attenuated neuronal damage and apoptosis in the hippocampus 72 h after SE. In addition, baicalin decreased SE-induced expression of miR-497 and cleaved caspase-3 protein, while upregulating the expression of Bcl-2 protein. In conclusion, the present results suggest that baicalin possesses potent antiapoptotic properties and attenuates hippocampal injury in mice after SE, which may be associated with the downregulation of miR-497 and cleaved caspase-3 and the upregulation of Bcl-2.

No MeSH data available.


Related in: MedlinePlus