Fig. 1: The expression level of LncRNA SNHG15 in high glucose-treated HUVECs and ischemic hind limbs of diabetic mice. | Laboratory Investigation

Fig. 1: The expression level of LncRNA SNHG15 in high glucose-treated HUVECs and ischemic hind limbs of diabetic mice.

From: LncRNA SNHG15 relieves hyperglycemia-induced endothelial dysfunction via increased ubiquitination of thioredoxin-interacting protein

Fig. 1

A SNHG15 expression was measured by qRT-PCR in HUVECs treated with 5, 15, or 25 mM d-glucose or 5 mM d-glucose + 20 mM mannitol. B SNHG15 expression was measured by qRT-PCR at 0, 12, 24, and 48 h after normal glucose (NG; 5 mM d-glucose) or high glucose (HG; 25 mM d-glucose) treatment of HUVECs. Unilateral femoral artery ligation was performed on diabetic (n = 25) and nondiabetic mice (n = 25). C Laser doppler perfusion imaging (LDPI) monitored the foot blood flow of ischemic (left) and nonischemic (right) hind limbs in diabetic and nondiabetic mice at five time-points (immediately after, and 7, 14, 21, 28 days after surgery). Mice were sacrificed at five time-points (immediately after, and 3, 7, 14, 28 days after surgery) and the gastrocnemius tissues of ischemic hind limbs in diabetic and nondiabetic mice were collected. n = 5 in each group. D SNHG15 expression was measured by qRT-PCR. E The primary endothelial cells (ECs) were isolated from gastrocnemius tissues of diabetic/nondiabetic mice’s ischemic hind limbs 28 days after surgery and the SNHG15 expression was measured. *P < 0.05, **P < 0.01, ***P < 0.001 vs NG-treated HUVECs or nondiabetic mice.

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