Scutellaria barbata attenuates diabetic retinopathy by preventing retinal inflammation and the decre

来源 :International Journal of Ophthalmology | 被引量 : 0次 | 上传用户:myjob3
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AIM: To observe the attenuation of ethanol extract of Herba Scutellaria barbata(SE) against diabetic retinopathy(DR) and its engaged mechanism.METHODS: C57BL/6J mice were intraperitoneally injected with streptozotocin(STZ, 55 mg/kg) for 5 consecutive days to induce diabetes. The diabetic mice were orally given with SE(100, 200 mg/kg) for 1mo at 1mo after STZ injection. Blood-retinal barrier(BRB) breakdown was detected by using Evans blue permeation assay. Real-time polymerase chain reaction(RT-PCR), Western blot and immunofluorescence staining were used to detect m RNA and protein expression. Enzyme-linked immunosorbent assay(ELISA) was used to detect serum contents of tumor necrosis factor-α(TNF-α) and interleukin(IL)-1β.RESULTS: SE(100, 200 mg/kg) reversed the breakdown of BRB in STZ-induced diabetic mice. The decreased expression of retinal claudin-1 and claudin-19, which are both tight junction(TJ) proteins, was reversed by SE. SE decreased the increased serum contents and retinal m RNA expression of TNF-α and IL-1β. SE also decreased the increased retinal expression of intercellular cell adhesion molecule-1(ICAM-1). SE reduced the increased phosphorylation of nuclear factor kappa B(NFκB) p65 and its subsequent nuclear translocation in retinas from STZinduced diabetic mice. Results of Western blot and retinal immunofluorescence staining of ionized calcium-binding adapter molecule 1(Iba1) demonstrated that SE abrogated the activation of microglia cells in STZ-induced diabetic mice.CONCLUSION: SE attenuates the development of DR by inhibiting retinal inflammation and restoring the decreased expression of TJ proteins including claudin-1 and claudin-19. AIM: To observe the attenuation of ethanol extract of Herba Scutellaria barbata (SE) against diabetic retinopathy (DR) and its engaged mechanism. METHODS: C57BL / 6J mice were intraperitoneally injected with streptozotocin (STZ, 55 mg / kg) to diabetic. The diabetic mice were orally given with SE (100, 200 mg / kg) for 1mo at 1mo after STZ injection. Blood-retinal barrier (BRB) breakdown was detected by using Evans blue permeation assay. Real- The enzyme-linked immunosorbent assay (ELISA) was used to detect the serum contents of tumor necrosis factor-a (TNF-α) and interleukin (RT-PCR), Western blot and immunofluorescence staining were used to detect m RNA and protein expression IL) -1β.RESULTS: SE (100, 200 mg / kg) reversed the breakdown of BRB in STZ-induced diabetic mice. The decreased expression of retinal claudin-1 and claudin-19, which are both tight junction (TJ) proteins , reversed it by SE. SE decreased the increased serum contents and retin SE also reduces the increased retinal expression of intercellular cell adhesion molecule-1 (ICAM-1). SE reduced the increased phosphorylation of nuclear factor kappa B (NFKB) p65 and its subsequent nuclear translocation in retinas from STZinduced diabetic mice. Results of Western blot and retinal immunofluorescence staining of ionized calcium-binding adapter molecule 1 (Iba1) demonstrated that SE abrogated the activation of microglia cells in STZ-induced diabetic mice. CONCLUSION: SE attenuates the development of DR by inhibiting retinal inflammation and restoring the decreased expression of TJ proteins including claudin-1 and claudin-19.
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