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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.

No MeSH data available.


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Neuronal apoptosis in hippocampal CA3 subfields showing 72 h following induction of SE. Representative images of (A) sham, (B) SE and (C) baicalin groups (magnification, ×4,000). (D) Graph showing the percentage of TUNEL-positive cells for each treatment group expressed as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. SE, status epilepticus.
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f2-etm-0-0-3461: Neuronal apoptosis in hippocampal CA3 subfields showing 72 h following induction of SE. Representative images of (A) sham, (B) SE and (C) baicalin groups (magnification, ×4,000). (D) Graph showing the percentage of TUNEL-positive cells for each treatment group expressed as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. SE, status epilepticus.

Mentions: TUNEL staining was used to evaluate apoptotic neuronal death in the hippocampal CA3 subfields of mice sacrificed 72 h following the induction of SE, processed as described, digested using proteinase K with chromosomal degradation visualized and using TdT followed by chromogen. Fig. 2 shows representative images of neuronal apoptosis in hippocampal CA3 subfields for each treatment group. Quantitative analysis of apoptotic nuclei as expressed as the percentage of apoptotic cells of the total revealed that the SE and baicalin groups had higher levels of TUNEL staining indicative of neuronal apoptosis compared with the sham group. By contrast, those that received baicalin treatment prior to SE had significantly lower levels of TUNEL staining than those that did not, indicating a suppression of SE-induced neuronal apoptosis (Fig. 2D) (P<0.05).


Effect of baicalin on hippocampal damage in kainic acid-induced epileptic mice
Neuronal apoptosis in hippocampal CA3 subfields showing 72 h following induction of SE. Representative images of (A) sham, (B) SE and (C) baicalin groups (magnification, ×4,000). (D) Graph showing the percentage of TUNEL-positive cells for each treatment group expressed as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. SE, status epilepticus.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f2-etm-0-0-3461: Neuronal apoptosis in hippocampal CA3 subfields showing 72 h following induction of SE. Representative images of (A) sham, (B) SE and (C) baicalin groups (magnification, ×4,000). (D) Graph showing the percentage of TUNEL-positive cells for each treatment group expressed as mean ± standard deviation (n=6 per group). *P<0.05 vs. sham group. †P<0.05 vs. SE group. SE, status epilepticus.
Mentions: TUNEL staining was used to evaluate apoptotic neuronal death in the hippocampal CA3 subfields of mice sacrificed 72 h following the induction of SE, processed as described, digested using proteinase K with chromosomal degradation visualized and using TdT followed by chromogen. Fig. 2 shows representative images of neuronal apoptosis in hippocampal CA3 subfields for each treatment group. Quantitative analysis of apoptotic nuclei as expressed as the percentage of apoptotic cells of the total revealed that the SE and baicalin groups had higher levels of TUNEL staining indicative of neuronal apoptosis compared with the sham group. By contrast, those that received baicalin treatment prior to SE had significantly lower levels of TUNEL staining than those that did not, indicating a suppression of SE-induced neuronal apoptosis (Fig. 2D) (P<0.05).

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