Anti-Inflammatory Effect Observed for Lutein

Lutein and Ischemic Injury

Lutein and its isomer, zeaxanthin, are carotenoids with antioxidant properties that are concentrated in ocular tissues, especially the retina. Observational studies have linked higher dietary intake levels of lutein and zeaxanthin to a decreased risk of AMD. Because these carotenoids absorb blue light, it's believed that they reduce photochemical damage that would otherwise occur in the retina when exposed to light of these wavelengths. However this may not be their only biochemical action, as new findings shed light on lutein's anti-inflammatory effects.

Retinal ischemia, or reduced blood flow to the retina, leads to neuronal cell death, which is seen in such conditions as retinal ischemic diseases, optic and diabetic neuropathies. Ischemic injury kills neurons by excitotoxicity (excessive glutamate), and also increases free radicals. Under ischemic conditions, excessive neuronal nitric oxide and the pro-inflammatory protein cyclo-oxygenase 2 (COX-2) are contributors to ischemia-mediated retinal cell death.

Study Design and Results

Investigators examined the effects of lutein on retinal ischemia, reported to be a good model for retinal neuronal cell death. High intraocular pressure was used to induce retinal ischemia in 8 week old Sprague-Dawley rats. The rats received an intravitreal injection of lutein (20% in corn oil) ½ hour before retinal ischemia was induced, while control animals were injected with corn oil only. Expression of COX-2 and neuronal nitric oxide synthetase (nNOS) was measured.

While the control group had an increased expression of these two proteins, lutein inhibited their expression in a dose-dependent manner. In addition, lutein was injected intraperitoneally 1 hour before and 1 hour after ischemia in another group. Compared to controls, survival of retinal neurons increased significantly to 85% in the ganglion cell layer and 88% in the inner cell layer. No difference in the protective effect of lutein was seen between the peritoneal and the vitreal routes of lutein administration (see figure 2).

Conclusions & Comments

"We have confirmed that nNOS and COX-2 expression are inhibited by lutein. These results suggest that lutein acts via two mechanisms: 1) an antioxidant effect and 2) direct inhibition of nNOS and COX-2 expression", wrote the lead investigators.

This study suggests a role for lutein in reducing damage caused by retinal ischemia and diabetic retinopathy - two diseases associated with oxidative stress caused by high intraocular pressure and high blood glucose levels, respectively. According to the lead author, "these results suggest that a lutein supplement may help protect against ischemia-mediated cell death in the retina".

Reference
Choi JS, et al. Inhibition of nNOS and COX-2 expression by lutein in acute retinal ischemia. Nutrition 22:608-71, 2006.