No abstract

The mouse lens capsular injury model has been widely used in investigating the mechanisms of anterior subcapsular cataract (ASC) and posterior capsule opacification (PCO), and evaluating the efficacy of antifibrotic compounds. Nevertheless, there is no available protocol to quantitatively assess the treatment outcomes. Our aim is to describe a new method that can successfully quantify the wound and epithelial-mesenchymal transition (EMT) markers expression in vivo. In this model, lens anterior capsule was punctured with a hypodermic needle, which triggered lens epithelial cells (LECs) proliferation and EMT rapidly. Immunofluorescent staining of injured lens anterior capsule whole-mounts revealed the formation of ASC and high expression of EMT markers in the subcapsular plaques. A series of sectional images of lens capsule were acquired from laser scanning confocal microscopy (LSCM) three-dimensional (3D) scanning. Using LSCM Image Browser software, we can not only obtain high resolution stereo images to present the spatial structures of ASC, but also quantify the subcapsular plaques and EMT markers distribution sucessfully. Moreover, we also demonstrated that histone deacetylases (HDACs) inhibitor TSA significantly prevented injury-induced ASC using this method. Therefore, the present research provides a useful tool to study ASC and PCO biology as well as the efficacy of new therapies.

No abstract

Human Angiostrongylus cantonensis (A. cantonensis) is a food-borne parasitic disease and can cause optic neuritis. Increasing clinical angiostrongyliasis cases with optic neuritis have been reported, but the pathogenesis has not been fully understood until now. Here, we applied rats with A. cantonensis infection as an animal model to study the pathogenesis of optic neuritis caused by the infection. We observed that the optic disk of experimental rats appeared hyperemic, the retina vein became thick, and the visual evoked potential (VEP) latency was prolonged. There were obvious inflammatory cell infiltration in the retina and optic nerve adventitia followed with obvious optic nerve fiber demyelination and retina ganglion swelling. We also evaluated the effect of dexamethasone combined with albendazole on optic neuritis of rats infected with A. cantonensis. The results showed it had no obvious effect to prevent progressive visual deterioration for optic neuritis caused by A. cantonensis. The studies provided evidence that the pathogenesis of optic neuritis in infected rats was correlated to optic nerve demyelination and ganglion cell damage caused by optic nerve inflammation, and the common therapy to this disease was not so effective. Based on the above results, it may be necessary to combine neuroprotective agents with common therapy to treat and protect optic nerve and ganglion cells from their secondary injury.

No abstract