Sanguiin H-11 from Sanguisorbae radix protects HT22 murine hippocampal cells against glutamate-induced death. Issue 2 (15th January 2019)

• Record Type: Journal Article
• Authors: Song, Ji Hoon; Kim, Song-Yi; Hwang, Gwi Seo; Kim, Youn-Sub; Kim, Hyun Young; Kang, Ki Sung
• Is Part Of: Bioorganic & medicinal chemistry letters. Volume 29:Issue 2(2019)
• Page Start: 252
• Page End: 256
• Publication Date: 2019-01-15
• Subjects: Sanguiin H-11 (SH-11) -- Glutamate -- Mitogen-activated protein kinase -- Oxidative stress -- HT22 cells; Bioorganic chemistry -- Periodicals; Pharmaceutical chemistry -- Periodicals; 572
• DOI: 10.1016/j.bmcl.2018.11.042
• Languages: English
• ISSNs: 0960-894X

Abstract

Graphical abstract: Highlights: Sanguiin-11 possessed a strong antioxidant activity. Sanguiin-11 prevented glutamate-induced death in HT22 cells. Sanguiin-11 inhibited oxidative stress-mediated MAPK activation. Abstract: Excessive glutamate level induces neuronal death in acute brain injuries and chronic neurodegenerative diseases. Natural compounds from medicinal and food plants have been attracting interest as a treatment for neurological disorders. Sanguiin H-11 (SH-11), a hydrolysable ellagitannin, inhibits neutrophil movement and nitric oxide -production. However, its neuroprotective effect has not been studied. Therefore, the present study examined the protective effect of SH-11 from Sanguisorbae radix and its mechanism against glutamate-induced death in HT22 cells. Our results showed that SH-11 possessed a strong antioxidant activity and prevented glutamate-induced death in HT22 cells. As a strong antioxidant, SH-11 significantly reduced glutamate-induced increases in intracellular reactive oxygen species accumulation and calcium ion influx. Western blotting analysis showed that glutamate-induced phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-related kinases 1/2, c-Jun N -terminal kinase, and p38, was significantly decreased by SH-11. Furthermore, SH-11 significantly decreased the number of annexin V-positive HT22 cells, which is indicating apoptotic cell death. In conclusion, our results suggested that SH-11 exerted a potent neuroprotective activity against glutamate-mediated apoptotic cell death by inhibiting oxidative stress-mediated MAPK activation.