Authors: Dong Shuqian, Liu Shuangzhen, Li Qiuming
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Objective
To investigate the role of leukemia inhibitory factor (LIF) on retinal photoreceptor cells and the underlying mechanism after light damage.
Methods
Fifty 5-6 weeks old BALB/c mice were randomly divided into normal control group (10 mice), light damage+ LIF group (20 mice) and light damage+ PBS group (20 mice). Four days before exposing to light, the right eye of each animal in light damage+ LIF group and light damage+ PBS group was injected with LIF and PBS, respectively; then the mice in the light damage+ LIF group and light damage+ PBS group were exposed to 4 000 lx intensity of cool white fluorescent light for 4 hours to establish the experimental model of retinal light damage.The function and morphology of retinal photoreceptor cells were detected by flash electroretinogram (fERG) and histopathological examination.Real-time PCR was used to detect the mRNA expression of Jak3, STAT3, and apoptosis-related factor Bcl-2 and Bax.The use of animals is guided by the State Science and Technology Commission’s regulations on the management of experimental animals.
Results
The amplitudes of scotopic ERG a wave of 0.01, 1, 100, 200, 400 cd·s/m2 light in the light damage+ PBS group were significantly lower than those in the normal control group and light damage+ LIF group (all at P<0.05). The amplitudes of photopic ERG b wave of different color light in the light damage+ PBS group were significantly lower than those in the normal control group and light damage+ LIF group (all at P<0.05). The number of photoreceptor nuclei in the light damage+ PBS group was significantly lower than that in the normal control group and light damage+ LIF group (both at P<0.05). Compared with light damage+ PBS group, the relative expression of Jak3, STAT3, Bcl-2 mRNA in light damage+ LIF group were significantly increased (all at P<0.05), and the relative expression of Bax mRNA were significantly decreased (P<0.05).
Conclusions
LIF can protect retinal photoreceptor cells from light damage, which may result from the activation of Jak3/STAT3 signaling pathway and inhibition of its downstream Bax/Bcl-2 apoptotic pathway.