Limits...
Chrysin protects against focal cerebral ischemia/reperfusion injury in mice through attenuation of oxidative stress and inflammation.

Yao Y, Chen L, Xiao J, Wang C, Jiang W, Zhang R, Hao J - Int J Mol Sci (2014)

Bottom Line: Our data show that chrysin successfully decreased neurological deficit scores and infarct volumes, compared with the vehicle group.Moreover, chrysin also inhibited the MCAO-induced up-regulation of nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the vehicle.These results suggest that chrysin could be a potential prophylactic agent for cerebral ischemia/reperfusion (I/R) injury mediated by its anti-inflammatory and anti-oxidative effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China. yaoy1986@gmail.com.

ABSTRACT
Inflammation and oxidative stress play an important part in the pathogenesis of focal cerebral ischemia/reperfusion (I/R) injury, resulting in neuronal death. The signaling pathways involved and the underlying mechanisms of these events are not fully understood. Chrysin, which is a naturally occurring flavonoid, exhibits various biological activities. In this study, we investigated the neuroprotective properties of chrysin in a mouse model of middle cerebral artery occlusion (MCAO). To this end, male C57/BL6 mice were pretreated with chrysin once a day for seven days and were then subjected to 1 h of middle cerebral artery occlusion followed by reperfusion for 24 h. Our data show that chrysin successfully decreased neurological deficit scores and infarct volumes, compared with the vehicle group. The increases in glial cell numbers and proinflammatory cytokine secretion usually caused by ischemia/reperfusion were significantly ameliorated by chrysin pretreatment. Moreover, chrysin also inhibited the MCAO-induced up-regulation of nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the vehicle. These results suggest that chrysin could be a potential prophylactic agent for cerebral ischemia/reperfusion (I/R) injury mediated by its anti-inflammatory and anti-oxidative effects.

Show MeSH

Related in: MedlinePlus

Effect of chrysin on neurological deficits, brain infarct volume and pathomorphological changes in mice with cerebral I/R injury. (A) Neurological score was measured in mice that underwent 1 h of ischemia followed by 24 h of reperfusion. Chrysin decreased the neurological score compared to the middle cerebral artery occlusion (MCAO) group; (B) Representative coronal brain sections stained with 1% TTC. Mice were subjected to 1 h of ischemia followed by 24 h of reperfusion; the infarct area is white; (C) Quantitative analysis of the percentage of brain infarct volume. Chrysin pretreatment diminished the percentage of brain infarct volume and there is a statistical difference compared with the MCAO group; (D) H&E staining showed that the normal morphologic features of neurons were present in the sham group. The MCAO group showed the loss of neurons and the presence of multiple vacuolated interspaces. Chrysin significantly ameliorated the damage of neurons that is associated with ischemia in the MCAO group (Magnified 20×). Data are expressed as means ± SEM, * p < 0.05, vs. MCAO group, n = 6.
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4264203&req=5

ijms-15-20913-f001: Effect of chrysin on neurological deficits, brain infarct volume and pathomorphological changes in mice with cerebral I/R injury. (A) Neurological score was measured in mice that underwent 1 h of ischemia followed by 24 h of reperfusion. Chrysin decreased the neurological score compared to the middle cerebral artery occlusion (MCAO) group; (B) Representative coronal brain sections stained with 1% TTC. Mice were subjected to 1 h of ischemia followed by 24 h of reperfusion; the infarct area is white; (C) Quantitative analysis of the percentage of brain infarct volume. Chrysin pretreatment diminished the percentage of brain infarct volume and there is a statistical difference compared with the MCAO group; (D) H&E staining showed that the normal morphologic features of neurons were present in the sham group. The MCAO group showed the loss of neurons and the presence of multiple vacuolated interspaces. Chrysin significantly ameliorated the damage of neurons that is associated with ischemia in the MCAO group (Magnified 20×). Data are expressed as means ± SEM, * p < 0.05, vs. MCAO group, n = 6.

Mentions: An examination of neurological function was carried out in mice subjected to 1 h of ischemia followed by 24 h of reperfusion. Compared with the MCAO group, the neurological deficit scores were significantly reduced in mice treated with chrysin (p < 0.05). The range of neurological deficit scores for the different groups is shown in Figure 1A. Representative brain slices showed that normal, viable brain tissues were stained deep red, while staining of the infarcted area was pale. No areas of infarction were observed in the sham group. The MCAO group had an obvious rise of infarct volume in comparison with the sham group. TTC staining (2,3,5-tripenyltetrazolium chloride) of brain sections following MCAO and reperfusion showed noticeable damage in the areas supplied by the middle cerebral artery. In comparison with the MCAO group, chrysin pretreatment significantly reduced the infarct volume (Figure 1B,C).


Chrysin protects against focal cerebral ischemia/reperfusion injury in mice through attenuation of oxidative stress and inflammation.

Yao Y, Chen L, Xiao J, Wang C, Jiang W, Zhang R, Hao J - Int J Mol Sci (2014)

Effect of chrysin on neurological deficits, brain infarct volume and pathomorphological changes in mice with cerebral I/R injury. (A) Neurological score was measured in mice that underwent 1 h of ischemia followed by 24 h of reperfusion. Chrysin decreased the neurological score compared to the middle cerebral artery occlusion (MCAO) group; (B) Representative coronal brain sections stained with 1% TTC. Mice were subjected to 1 h of ischemia followed by 24 h of reperfusion; the infarct area is white; (C) Quantitative analysis of the percentage of brain infarct volume. Chrysin pretreatment diminished the percentage of brain infarct volume and there is a statistical difference compared with the MCAO group; (D) H&E staining showed that the normal morphologic features of neurons were present in the sham group. The MCAO group showed the loss of neurons and the presence of multiple vacuolated interspaces. Chrysin significantly ameliorated the damage of neurons that is associated with ischemia in the MCAO group (Magnified 20×). Data are expressed as means ± SEM, * p < 0.05, vs. MCAO group, n = 6.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4264203&req=5

ijms-15-20913-f001: Effect of chrysin on neurological deficits, brain infarct volume and pathomorphological changes in mice with cerebral I/R injury. (A) Neurological score was measured in mice that underwent 1 h of ischemia followed by 24 h of reperfusion. Chrysin decreased the neurological score compared to the middle cerebral artery occlusion (MCAO) group; (B) Representative coronal brain sections stained with 1% TTC. Mice were subjected to 1 h of ischemia followed by 24 h of reperfusion; the infarct area is white; (C) Quantitative analysis of the percentage of brain infarct volume. Chrysin pretreatment diminished the percentage of brain infarct volume and there is a statistical difference compared with the MCAO group; (D) H&E staining showed that the normal morphologic features of neurons were present in the sham group. The MCAO group showed the loss of neurons and the presence of multiple vacuolated interspaces. Chrysin significantly ameliorated the damage of neurons that is associated with ischemia in the MCAO group (Magnified 20×). Data are expressed as means ± SEM, * p < 0.05, vs. MCAO group, n = 6.
Mentions: An examination of neurological function was carried out in mice subjected to 1 h of ischemia followed by 24 h of reperfusion. Compared with the MCAO group, the neurological deficit scores were significantly reduced in mice treated with chrysin (p < 0.05). The range of neurological deficit scores for the different groups is shown in Figure 1A. Representative brain slices showed that normal, viable brain tissues were stained deep red, while staining of the infarcted area was pale. No areas of infarction were observed in the sham group. The MCAO group had an obvious rise of infarct volume in comparison with the sham group. TTC staining (2,3,5-tripenyltetrazolium chloride) of brain sections following MCAO and reperfusion showed noticeable damage in the areas supplied by the middle cerebral artery. In comparison with the MCAO group, chrysin pretreatment significantly reduced the infarct volume (Figure 1B,C).

Bottom Line: Our data show that chrysin successfully decreased neurological deficit scores and infarct volumes, compared with the vehicle group.Moreover, chrysin also inhibited the MCAO-induced up-regulation of nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the vehicle.These results suggest that chrysin could be a potential prophylactic agent for cerebral ischemia/reperfusion (I/R) injury mediated by its anti-inflammatory and anti-oxidative effects.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin 300052, China. yaoy1986@gmail.com.

ABSTRACT
Inflammation and oxidative stress play an important part in the pathogenesis of focal cerebral ischemia/reperfusion (I/R) injury, resulting in neuronal death. The signaling pathways involved and the underlying mechanisms of these events are not fully understood. Chrysin, which is a naturally occurring flavonoid, exhibits various biological activities. In this study, we investigated the neuroprotective properties of chrysin in a mouse model of middle cerebral artery occlusion (MCAO). To this end, male C57/BL6 mice were pretreated with chrysin once a day for seven days and were then subjected to 1 h of middle cerebral artery occlusion followed by reperfusion for 24 h. Our data show that chrysin successfully decreased neurological deficit scores and infarct volumes, compared with the vehicle group. The increases in glial cell numbers and proinflammatory cytokine secretion usually caused by ischemia/reperfusion were significantly ameliorated by chrysin pretreatment. Moreover, chrysin also inhibited the MCAO-induced up-regulation of nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the vehicle. These results suggest that chrysin could be a potential prophylactic agent for cerebral ischemia/reperfusion (I/R) injury mediated by its anti-inflammatory and anti-oxidative effects.

Show MeSH
Related in: MedlinePlus