Soo-Jin Kim1,2, Mi-Sun Sung1, Hwan Heo1, Jae-Hyuk Lee3,2, Sang-Woo Park1,2. 1. a Department of Ophthalmology , Chonnam National University Medical School & Hospital , Gwangju , Korea . 2. c Department of Pathology , Chonnam National University Medical School , Gwangju , Korea. 3. b Center for Creative Biomedical Scientists at Chonnam National University, Chonnam National University Medical School , Gwangju , Korea and.
Abstract
PURPOSE: To investigate whether mangiferin can increase the viability of retinal ganglion cells (RGCs) in ischemic mouse retina, and to determine the possible mechanism of neuroprotection. METHODS: C57BL/6J mice underwent constant elevation of intraocular pressure for 60 min and received saline or mangiferin (30 mg/kg) intraperitoneally once daily until sacrifice. HIF-1α, GFAP and SIRT1 expression was assessed at 1, 4, and 7 days after retinal ischemia. Bax and Bcl-2 expression was also analyzed at 1 and 4 days. RGC survival was assessed by labeling flat-mounted retinas with Brn3a at 2 weeks after retinal ischemia. The effect of co-treatment with mangiferin and sirtinol (SIRT1 inhibitor) was also evaluated. RESULTS: The expression of HIF-1α and GFAP was upregulated in saline-treated retinas within 7 days after ischemia. Mangiferin treatment suppressed this upregulation. The expression of SIRT1 was downregulated in saline-treated ischemic retinas. This downregulation was reversed by mangiferin treatment, resulting in a significant difference from saline-treated ischemic retinas. In mangiferin-treated ischemic retinas, Bax expression was downregulated, whereas Bcl-2 expression was upregulated in comparison with saline-treated ischemic retinas. Mangiferin treatment protected ischemic retinas against RGC loss. Treatment of sirtinol decreased the neuroprotective effect of mangiferin. CONCLUSIONS: Our findings suggest that mangiferin has a neuroprotective effect on RGC through downregulation of HIF-1a and GFAP, and upregulation of SIRT1 in ischemic mouse retinas. We suggest that mangiferin might be a potential neuroprotective agent against RGC loss under oxidative stress.
PURPOSE: To investigate whether mangiferin can increase the viability of retinal ganglion cells (RGCs) in ischemicmouse retina, and to determine the possible mechanism of neuroprotection. METHODS: C57BL/6J mice underwent constant elevation of intraocular pressure for 60 min and received saline or mangiferin (30 mg/kg) intraperitoneally once daily until sacrifice. HIF-1α, GFAP and SIRT1 expression was assessed at 1, 4, and 7 days after retinal ischemia. Bax and Bcl-2 expression was also analyzed at 1 and 4 days. RGC survival was assessed by labeling flat-mounted retinas with Brn3a at 2 weeks after retinal ischemia. The effect of co-treatment with mangiferin and sirtinol (SIRT1 inhibitor) was also evaluated. RESULTS: The expression of HIF-1α and GFAP was upregulated in saline-treated retinas within 7 days after ischemia. Mangiferin treatment suppressed this upregulation. The expression of SIRT1 was downregulated in saline-treated ischemic retinas. This downregulation was reversed by mangiferin treatment, resulting in a significant difference from saline-treated ischemic retinas. In mangiferin-treated ischemic retinas, Bax expression was downregulated, whereas Bcl-2 expression was upregulated in comparison with saline-treated ischemic retinas. Mangiferin treatment protected ischemic retinas against RGC loss. Treatment of sirtinol decreased the neuroprotective effect of mangiferin. CONCLUSIONS: Our findings suggest that mangiferin has a neuroprotective effect on RGC through downregulation of HIF-1a and GFAP, and upregulation of SIRT1 in ischemicmouse retinas. We suggest that mangiferin might be a potential neuroprotective agent against RGC loss under oxidative stress.
Authors: Ahmara G Ross; Brahim Chaqour; Devin S McDougald; Kimberly E Dine; Thu T Duong; Ryan E Shindler; Jipeng Yue; Tehui Liu; Kenneth S Shindler Journal: Biomolecules Date: 2022-06-14
Authors: Sean M Silverman; Byung-Jin Kim; Garreth R Howell; Joselyn Miller; Simon W M John; Robert J Wordinger; Abbot F Clark Journal: Mol Neurodegener Date: 2016-03-24 Impact factor: 14.195