Abstract

Irreversible loss of retinal ganglion cells (RGCs) is a common pathological feature of various optic nerve degenerative diseases such as glaucoma and ischemic optic neuropathy. Effective protection of RGCs is the key to successful treatment of these diseases. Total Panax notoginseng saponins (TPNS) are the main active component of Panax notoginseng, which has an inhibitory effect on the apoptosis pathway. This study is aimed at assessing the protective effect of TPNS on RGCs of the optic nerve crush (ONC) model of rats and exploring the underlying mechanisms. The intraperitoneal or intravitreal injection of TPNS was used based on the establishment of the rat ONC model. Fifteen days after the injury, the cell membrane fluorescent probe (Fluoro-Gold) was applied to retrograde RGCs through the superior colliculus and obtain the number of surviving RGCs. TUNEL assay was also used to detect the number and density of RGC apoptosis after the ONC model. The expression and distribution of Bcl-2/Bax, c-Jun/P-c-Jun, and P-JNK in the retina were demonstrated by Western blot analysis. After the intervention of TPNS, the rate of cell survival increased in different retinal regions (p < 0.05) and the number of apoptosis cells decreased. Regarding the expression of Bcl-2/Bax, c-Jun/P-c-Jun, and P-JNK-related apoptotic proteins, TPNS can reduce the level of apoptosis and play a role in protecting RGCs (p < 0.05). These findings indicate that topical administration of TPNS can inhibit cell apoptosis and promote RGC survival in the crushed optic nerve.

Highlights

  • Optic nerve damage is the main cause of irreversible visual impairment

  • After fifteen days of optic nerve crush (ONC) accompanied by regular drug administration, bilateral superior colliculus retrograde Fluoro-Gold labeling and retinal ganglion cells (RGCs) counting were performed (Figure 3(a))

  • The results presented that Total Panax notoginseng saponins (TPNS) effectively improved the survival number of RGCs in the ONC rats

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Summary

Introduction

Optic nerve damage is the main cause of irreversible visual impairment. The mechanism is that degenerated axons lead to the gradual death of retinal ganglion cells (RGCs) [1, 2]. Optic neuropathy can cause color vision changes and abnormal visual fields. Visual information is transmitted from the eyes to the brain through the axons of RGCs. The optic nerve is made up of 1.2 million axons emitted by RGCs [3]. It is conceivable that RGCs has a very close relationship with the optic nerve. Common optic nerve diseases include glaucomatous optic neuropathy, ischemic neuropathy, and inflammatory neuropathy[4]

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