Jingdong LIU, Sha CHEN, Yuchun WANG, et al. β-caryophyllene improves cerebral ischemia reperfusion injury in rats via Notch1/NF-κB signal axis[J]. Journal of Third Military Medical University, 2021, 43(3): 218-225.
DOI:
Jingdong LIU, Sha CHEN, Yuchun WANG, et al. β-caryophyllene improves cerebral ischemia reperfusion injury in rats via Notch1/NF-κB signal axis[J]. Journal of Third Military Medical University, 2021, 43(3): 218-225. DOI: 10.16016/j.1000-5404.202009067.
β-caryophyllene improves cerebral ischemia reperfusion injury in rats via Notch1/NF-κB signal axis
To explore the protective effect of β-caryophyllene (BCP) on cerebral ischemia-reperfusion (I/R) rats and related mechanism.
Methods
2
SD rats were randomized into sham operation group
I/R group
and low-
medium- and high-dose BCP groups (102
204 and 408 mg·kg
-1
)
Jagged1 (Notch1 agonist
50 mg·kg
-1
in 3 h before I/R injury)+BCP group
and Jagged1 group. The treatments were given to the corresponding rats through intragastric infusion. In 7 d later
SD rat CIR model was established with suture-occlusion
with ischemia for 1.5 h followed by reperfusion for 48 h. The infarct volume and neurobehavioral s
core were measured; Western blotting was used to detect the cerebral protein levels of Notch1
NF-κB p65
NF-κB p-p65 and Hes1; HE staining was applied to observe the number of dead cells
and ELISA was employed to detect the changes of TNF-α and IL1-β contents in the ischemic hippocampus.
Results
2
BCP treatment could significantly improve the neurological deficit
reduce the infarct volume
down-regulate the protein levels of Notch1
NF-κB and Hes1 in the hippocampus (
P
<
0.05)
reduce the releases of TNF-α and IL-1β (
P
<
0.05)
and attenuate the death of hippocampal neuronal cells in the rats after cerebral I/R injury. Comparing the simple Jagged1 intervention group
Notch1 agonist
Jagged1
could antagonize the therapeutic effects of BCP.
Conclusion
2
BCP can attenuate cerebral I/R injury in rats
and exerts its protective effect probably through inhibiting Notch1/NF-κB signal axis to reduce the release of inflammatory factors.
关键词
Keywords
references
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