Reperfusion Injury and Luteolin

I found the basic science article about Leukocyte accumulation in reperfusion injury after stroke to be pretty interesting so I went and found another article that has to do with reperfusion injury. The paper I read was title “Postischemic administration of liposome-encapsulated luteolin prevents against ischemia-reperfusion injury in a rat middle cerebral artery occlusion (MACO) model” (long title I know). Luteolin is a flavonoid (also collectively known as Vitamin P and citrin)that from preliminary research is thought to have a role as an antioxidant, a free radical scavenger, or an immune system modulator. In basic research results show it could also work as an anti-inflammatory agent.

This study was done by taking a group of female rats and dividing them it to four different groups. These groups were: sham group with liposome solvent, model group with liposome solvent, treatment group with 5mg/kg lipLU, and treatment group with 20mg/kg lipLU (lipLU = liposome-encapsulated luteolin). They performed a MACO on all groups except for the sham group, the filament was removed 40 minutes after induction of ischemia. Some of the rats were killed in order to look at brain slices.

What they found was that when multiple administration of lipLU beginning at 6 hour post reperfusion showed a decrease in the symptom score and pronounced enhancement of balance score on day 7 (in comparison to those rats without lipLU) and there were even more behavioral improvements by day 14. This showed that the lipLU possessed a long lasting anti ischemic activity, they confirmed this by looking at brain slices that showed delayed action in improvement of the histological injury after treatment. The study also showed that with the ischemic attach and reperfusion (I/R) there was an increase of reactive oxygen species (ROS) and a inhibition of endogenous antioxidant defense system (CAT and GSH) showing an imbalance between the species. With those treated with lipLU conferred reversing actions on the increase in ROS production and on the decrease of endogenous antioxidant GSH and CAT activity. The researchers say that this is what is improving the brain damage by rebalancing the pro-oxidant/antioxidant force.

This study shows that luteolin acts by neroprotection in primary cultured neurons exposed to oxidative stress and anti-ischemia in animals insulted by I/R (Zhao 7). I think that this study is a good start and that this luteolin should be studied more in the future so that the exact mechanisms can be found and to see how it would translate to human models.

References:

Zhao, Gang, Shao-Yun Zang etal. "Postischemic Administration of Liposome-
encapsulated Luteolin Prevents Aganist Ischemia-reperfusion Injury in a Rat
Middle Cerebral Artery Occlusion Model." Journal of Nutritional Biochemistry
(2010): 1-8. Print.