ABSTRACT
Glaucoma is a common blinding eye disease characterized by progressive loss of retinal ganglion cells （RGCs） and their axons， gradual loss of visual field， and optic atrophy. The pathological changes of glaucoma are mainly the degeneration， atrophy， and loss of RGCs and their axons， which can eventually lead to the permanent impairment of visual function. The specific pathogenesis of glaucoma remains unclear. Autophagy is a process in which damaged， denatured， or senescent proteins and organelles are transported to lysosomes for digestion and degradation in order to continuously renew and rebuild cells for reuse. As revealed by clinical case analysis and animal experiments， Chinese patent medicine and some traditional Chinese medicine （TCM） therapies may be able to target the autophagy pathway. This paper expounded the role of autophagy in glaucoma-induced ocular hypertension and optic nerve injury from the aspects of stress response of ocular tissue to high intraocular pressure， trabecular meshwork dysfunction， immune regulation， and scar regulation as well as the regulatory effects of some Chinese medicinal ingredients on autophagy， aiming to explore the possibility of integrated TCM and western medicine in regulating autophagy and preventing glaucoma-induced optic nerve injury and early visual field loss. It was found that Chinese medicinal monomers or extracts function via multiple pathways and multiple targets， mainly involving two classical autophagy pathways， namely phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） and adenosine monophosphate-activated protein kinase （AMPK）. Moreover， the current studies on the neuroprotective effect of TCM mostly focus on the brain and spinal cord lesions of the central nervous system， and its protective mechanism against optic nerve injury in glaucoma still needs further investigation. In addition， autophagy was like a "double-edged sword" in different experimental animal models and methods. How to artificially intervene in autophagy to prevent the apoptosis of RGCs and protect the optic nerve injury is still an urgent problem to be solved in the future research.
ABSTRACT
<p><b>OBJECTIVE</b>To obtain monoclonal antibodies (mAb) against LI-cadherin and investigate their effects on the proliferation of human hepatocellular carcinoma cells.</p><p><b>METHODS</b>Balb/c mice were immunized with recombinant LI-cadherin, and hybridoma cell lines secreting monoclonal antibodies against LI-cadherin were established with routine cell fusion and subcloning approach. The specificity of these mAbs was determined by enzyme-linked immunosorbent assay (ELISA) and Western blotting. The effect of the mAbs obtained on the growth of HepG2 cells was assessed using inverted microscope and MTT assay.</p><p><b>RESULTS</b>Two hybridoma cell lines (F001 and F002) stably secreting specific mAbs were obtained. Western blot analysis showed that the two antibodies specifically recognized LI-cadherin antigen derived from human eucaryotic cells or tissue. Treatment of the HepG2 cells with the mAbs resulted in reduced viable cell number and changes in the cell morphologies, and the two mAbs inhibited the proliferation of HepG2 cells in a concentration-dependent manner (P<0.05).</p><p><b>CONCLUSION</b>The two specific mAbs obtained can inhibit the proliferation of HepG2 cells in vitro, which facilitates further study of the relationship between LI-cadherin and tumors.</p>