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1.
Chinese Journal of Experimental Ophthalmology ; (12): 88-92, 2019.
Article in Chinese | WPRIM | ID: wpr-733650

ABSTRACT

Objective To study the expression of collapsin response mediator protein 2 (CRMP-2) in the visual cortex of monocular form deprivation amblyopia rats.Methods Sixty-four 14-day-old rats were randomly divided into monocular deprivation amblyopia group and normal control group by random number table method.Right eyelid margin suture was performed at 14 days after birth in the monocular deprivation amblyopia group.Eight rats in the monocular deprivation amblyopia group and the normal control group were observed at 14,21,45 and 120 days after birth,respectively.Flash visual evoked potential (F-VEP) was used to dectect the latency and amplitude of P1 wave.The expression of CRMP-2 in visual cortex was observed by immunohistochemical method.The use and care of the animals complied with Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission.This study protocol was approved by Ethic Committee of the University of South China (No.20140228).Results F-VEP results showed that the amplitudes of P1 were decreased and latent periods of P1 were prolonged in the monocular deprivation amblyopia group compared with the normal control group (t=16.760,P =0.000;t =-22.919,P =0.000).CRMP-2 expression levels in the visual cortex of monocular deprivation amblyopia groups and normal control groups were compared at different time points after birth,and the differences were statistically significant (Fgroup =8.855,P =0.010;Ftime =63.091,P =0.000).Compared with normal control groups,the expressions of CRMP-2 at the postnatal 21,45 and 120 days were obviously decreased in the monocular deprivation amblyopia groups,the differences were statistically significant (all at P<0.05).Conclusions CRMP-2 may be involved in the occurrence and development of amblyopia.

2.
Recent Advances in Ophthalmology ; (6): 230-234, 2017.
Article in Chinese | WPRIM | ID: wpr-511137

ABSTRACT

Objective To dynamically observe the expressions of Toll like-receptor 2 (TLR-2),TLR-4 and inflammatory cytokine IL-1 beta and TNF alpha,and analyze the correlation between TLR-2,TLR-4 and inflammatory response on rat cornea alkali burn.Methods Forty SPF healthy SD rats were excluded the anterior segment disease,the right eye was set as burn experiment and the left eye as normal control,Ⅲ level corneal alkali burn model was established with concentration of 1 mol · L-1 NaOH(At the establishment and after the establishment of the model,the inconsistent degree of corneal bums,the corneal perforation and hyphema in rats,etc.,were removed,and finally randomly selected 32 eligible rats),then were randomly grouped into 3 days,7 days,14 days and 21 days group,8 eyes in each group.The rats were observed and photographed anterior segment of each group,evaluated the corneal inflammation index,then removed the eyeball of the rats in the corresponding time points.The eyeballs were made into pathological tissue section and stained with HE method.The number of inflammatory cells in the cornea was calculated,and the expression of TLR-2,TLR-4,IL-1 beta and TNF alpha was detected in the rat cornea with method of Western blot protein detection at the same time.The differences of each group were analyzed,and the correlation was assessed between TLRs and inflammatory factor.Results There were the expressions of TLR-2,TLR-4,IL-1 beta and TNF alpha in the normal rat cornea,and its expressions were gradually increased after alkali burn,reached the peak at the 7 days,then decreased gradually,the difference of each group (the 3 day,the 7 day,the 14 day,the 21 day) was statistically significant (all P < 0.05).The expressions of TLR-2 and IL-1 beta (r =0.986,P < 0.05),TNF alpha (r =0.986,P < 0.05) were positive correlated.The expressions of TLR-4 and IL-1 beta(r =0.975,P < 0.05),TNF alpha (r =0.990,P <0.05) were positive correlated.Conclusion TLRs participates and may start immune inflammatory response after corneal alkali burn,mediates the production of inflammatory cytokine.

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