Roots of Lithospermum erythrorhizon promotes retinal cell survival in optic nerve crush-induced retinal degeneration.

Affiliation

Kang TK(1), Le TT(2), Kim KA(3), Kim YJ(1), Lee WB(4), Jung SH(5).
Author information:
(1)Natural Product Research Center, Korea Institute of Science & Technology, Gangneung, 25451, Republic of Korea.
(2)Natural Product Research Center, Korea Institute of Science & Technology, Gangneung, 25451, Republic of Korea; Division of Bio-Medical Science & Technology, KIST School, Korea University of Science and Technology, Gangneung, 25451, Republic of Korea.
(3)Division of Medical Oncology, Yonsei Cancer Center, Department of Internal Medicine, Yonsei University, Republic of Korea.
(4)Natural Product Research Center, Korea Institute of Science & Technology, Gangneung, 25451, Republic of Korea. Electronic address: [Email]
(5)Natural Product Research Center, Korea Institute of Science & Technology, Gangneung, 25451, Republic of Korea; Division of Bio-Medical Science & Technology, KIST School, Korea University of Science and Technology, Gangneung, 25451, Republic of Korea. Electronic address: [Email]

Abstract

Lithospermum erythrorhizon (L. erythrorhizon), used in traditional medicine, is a potent wound healing, anti-inflammatory and antioxidant plant. However, the effects of L. erythrorhizon on retinal degenerative diseases remain unknown. Here, we explored the protective effects of L. erythrorhizon in in vitro and in vivo retinal degeneration. We found that ethanol extract of L. erythrorhizon (EELE) and the dichloromethane fraction of L. erythrorhizon (MCLE) significantly increased cell viability under glutamate/BSO-induced excitotoxicity/oxidative stress in R28 cells. Treatment with EELE and MCLE reduced the intracellular reactive oxygen species (ROS) and the levels of apoptotic proteins, such as cleaved PARP and cleaved caspase-3. Furthermore, oral administration of EELE and MCLE in an in vivo optic nerve crush mouse model decreased RGC cell death and increased retinal thickness. The major compound between EELE and MCLE was found to be lithospermic acid A (LAA), which has been shown to prevent the elevation of ROS in R28. Therefore, EELE and MCLE have protective effects against the death of retinal cells in vitro and in vivo, and the major compound, LAA, has an antioxidant effect on retinal cells, suggesting that EELE and MCLE could be beneficial agents for retinal degenerative diseases, including glaucoma.