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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.


Related in: MedlinePlus

Photomicrographs showing cell morphology 72 h following status epilepticus (SE) induction (magnification, ×200; stain, hematoxylin and eosin). Regions within the hippocampal (A-C) CA1 and (D-F) CA3 subfields shown at magnification, ×200. (A and D) Neurons from sham animals and (B and E) neurons from seizure-induced injury. (A) Arrows in 1a indicates shrunken neurons. (E) Arrow indicates an empty space known as cavitation, implying the formation of vapor cavities. (C and F) HE staining indicated that SE-induced neuronal injury in the hippocampal CA1 and CA3 subfields were markedly reduced by 100 mg/kg baicalin. The arrow in 1B indicates shrunken neurons.
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f1-etm-0-0-3461: Photomicrographs showing cell morphology 72 h following status epilepticus (SE) induction (magnification, ×200; stain, hematoxylin and eosin). Regions within the hippocampal (A-C) CA1 and (D-F) CA3 subfields shown at magnification, ×200. (A and D) Neurons from sham animals and (B and E) neurons from seizure-induced injury. (A) Arrows in 1a indicates shrunken neurons. (E) Arrow indicates an empty space known as cavitation, implying the formation of vapor cavities. (C and F) HE staining indicated that SE-induced neuronal injury in the hippocampal CA1 and CA3 subfields were markedly reduced by 100 mg/kg baicalin. The arrow in 1B indicates shrunken neurons.

Mentions: Morphological examination was performed on sections cut from brains removed 72 h following SE onset, fixed with 4% paraformaldehyde and stained using HE. As shown in Fig. 1, the majority of neurons in the hippocampal CA1 and CA3 subfields of mice in the SE group appeared shrunken with eosinophilic cytoplasm, triangulated pyknotic nuclei and cavitation (empty holes indicative of vapor cavities; Fig. 1B and E). In the sham control group, there was no evidence of neuronal damage, with a lack of eosinophilic cytoplasm or triangulated pyknotic nuclei evident in the brains of mice in the SE group (Fig. 1A and D). Additionally, while mice that received baicalin (100 mg/kg) prior to SE showed eosinophilic cytoplasm and triangulated pyknotic nuclei indicative of SE induced neuronal damage, the number of damaged cells in the same areas was reduced compared to SE mice who did not receive baicalin (Fig. 1C and F).


Effect of baicalin on hippocampal damage in kainic acid-induced epileptic mice
Photomicrographs showing cell morphology 72 h following status epilepticus (SE) induction (magnification, ×200; stain, hematoxylin and eosin). Regions within the hippocampal (A-C) CA1 and (D-F) CA3 subfields shown at magnification, ×200. (A and D) Neurons from sham animals and (B and E) neurons from seizure-induced injury. (A) Arrows in 1a indicates shrunken neurons. (E) Arrow indicates an empty space known as cavitation, implying the formation of vapor cavities. (C and F) HE staining indicated that SE-induced neuronal injury in the hippocampal CA1 and CA3 subfields were markedly reduced by 100 mg/kg baicalin. The arrow in 1B indicates shrunken neurons.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-etm-0-0-3461: Photomicrographs showing cell morphology 72 h following status epilepticus (SE) induction (magnification, ×200; stain, hematoxylin and eosin). Regions within the hippocampal (A-C) CA1 and (D-F) CA3 subfields shown at magnification, ×200. (A and D) Neurons from sham animals and (B and E) neurons from seizure-induced injury. (A) Arrows in 1a indicates shrunken neurons. (E) Arrow indicates an empty space known as cavitation, implying the formation of vapor cavities. (C and F) HE staining indicated that SE-induced neuronal injury in the hippocampal CA1 and CA3 subfields were markedly reduced by 100 mg/kg baicalin. The arrow in 1B indicates shrunken neurons.
Mentions: Morphological examination was performed on sections cut from brains removed 72 h following SE onset, fixed with 4% paraformaldehyde and stained using HE. As shown in Fig. 1, the majority of neurons in the hippocampal CA1 and CA3 subfields of mice in the SE group appeared shrunken with eosinophilic cytoplasm, triangulated pyknotic nuclei and cavitation (empty holes indicative of vapor cavities; Fig. 1B and E). In the sham control group, there was no evidence of neuronal damage, with a lack of eosinophilic cytoplasm or triangulated pyknotic nuclei evident in the brains of mice in the SE group (Fig. 1A and D). Additionally, while mice that received baicalin (100 mg/kg) prior to SE showed eosinophilic cytoplasm and triangulated pyknotic nuclei indicative of SE induced neuronal damage, the number of damaged cells in the same areas was reduced compared to SE mice who did not receive baicalin (Fig. 1C and F).

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.


Related in: MedlinePlus