Effects of propofol pretreatment on microglial pyroptosis in the ischemic penumbra of rats subjected to cerebral ischemia-reperfusion
By: Ying, Pengdan
.
Contributor(s): Liu, Shurong.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2023Edition: Vol.85(4), Jul-Aug.Description: 1077-1084p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical sciencesSummary: To investigate the effect of propofol pretreatment on microglial pyroptosis in the ischemic penumbra of rats
subjected to cerebral ischemia-reperfusion. 90 rats were randomly divided into Sham group, model group,
nod-like receptor protein 3 inhibitor group, propofol low dose group and high dose group. Pathological
changes in the hippocampal region of the ischemic penumbra of brain tissue were observed by hematoxylin
and eosin staining; interleukin-1 beta and interleukin-18 levels were detected in the ischemic penumbra of
cerebral tissue by enzyme-linked immunosorbent assay; immunofluorescence double staining was performed
to detect the immunopositive co-expression of nod-like receptor protein 3, aspartate specific caspase 1 and
ionized calcium adaptor protein 1 in the ischemic penumbra of cerebral tissue. Compared with the model
group, the nod-like receptor protein 3 inhibitor group, propofol low dose group and propofol high dose group
groups also had significantly lower neurological deficit scores, cerebral infarction volumes, and interleukin-1
beta and interleukin-18 levels, ionized calcium adaptor protein 1/nod-like receptor protein 3, ionized calcium
adaptor protein 1/caspase 1 immunopositive co-expression, nod-like receptor protein 3, pro-caspase 1, P10,
P20 and interleukin-1 beta protein expressions in the ischemic penumbra were significantly reduced (p<0.05),
the pathological damage was improved to various degrees, and the number of nerve cells was increased. The
neuroprotective effect of propofol pretreatment on cerebral ischemia-reperfusion injury may be related to
the inhibition of microglial pyroptosis mediated by nod-like receptor protein 3 inflammasome.
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
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Articles Abstract Database
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School of Pharmacy Archieval Section | Not for loan | 2024-0417 |
To investigate the effect of propofol pretreatment on microglial pyroptosis in the ischemic penumbra of rats
subjected to cerebral ischemia-reperfusion. 90 rats were randomly divided into Sham group, model group,
nod-like receptor protein 3 inhibitor group, propofol low dose group and high dose group. Pathological
changes in the hippocampal region of the ischemic penumbra of brain tissue were observed by hematoxylin
and eosin staining; interleukin-1 beta and interleukin-18 levels were detected in the ischemic penumbra of
cerebral tissue by enzyme-linked immunosorbent assay; immunofluorescence double staining was performed
to detect the immunopositive co-expression of nod-like receptor protein 3, aspartate specific caspase 1 and
ionized calcium adaptor protein 1 in the ischemic penumbra of cerebral tissue. Compared with the model
group, the nod-like receptor protein 3 inhibitor group, propofol low dose group and propofol high dose group
groups also had significantly lower neurological deficit scores, cerebral infarction volumes, and interleukin-1
beta and interleukin-18 levels, ionized calcium adaptor protein 1/nod-like receptor protein 3, ionized calcium
adaptor protein 1/caspase 1 immunopositive co-expression, nod-like receptor protein 3, pro-caspase 1, P10,
P20 and interleukin-1 beta protein expressions in the ischemic penumbra were significantly reduced (p<0.05),
the pathological damage was improved to various degrees, and the number of nerve cells was increased. The
neuroprotective effect of propofol pretreatment on cerebral ischemia-reperfusion injury may be related to
the inhibition of microglial pyroptosis mediated by nod-like receptor protein 3 inflammasome.
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