The purpose of the present study was to determine whether the flavonoid, baicalin is effective at blunting the negative influence of ischemia/reperfusion to the rat retina
in situ and of various ...insults to a transformed retinal ganglion cells (RGC-5 cells) in culture.
Baicalin was administered intraperitoneally just before and after an ischemic insult to retina of one eye of a rat. Ischemia was delivered by raising the intraocular pressure above the systolic blood pressure for 50
min. Seven days after ischemia, retinas were analysed for the localisation of various antigens. Retinal extracts were also analysed for various mRNAs. Moreover, the content of specific proteins was deduced in retinal and optic nerve extracts. Also, RGC-5 cells in culture were given one of three different insults, light (1000
lx for 2 days), hydrogen peroxide (200
μM H
2O
2 for 24
h) or serum deprivation (48
h) where cell survival and reactive oxygen species (ROS) formation was assayed. Moreover, a lipid peroxidation assay was used to compare the antioxidant capacity of baicalin with the flavonoid, epigallocatechin gallate (EGCG).
Ischemia/reperfusion to the retina affected the localisation of Thy-1 and choline acetyltransferase (ChAT) and the content of various proteins (optic nerve and retina) and mRNAs (retina). Importantly, baicalin statistically blunted most of the effects induced by ischemia/reperfusion. Only the increase in caspase-8 and caspase-3 mRNAs caused by ischemia/reperfusion were unaffected by baicalin treatment. Baicalin also attenuated significantly the negative insult of light, hydrogen peroxide and serum withdrawal to RGC-5 cells. In the lipid peroxidation studies, baicalin was also found to be equally effective as EGCG to act as an antioxidant. Significantly, the negative insult of serum withdrawal on RGC-5 cell survival was blunted by baicalin but not by EGCG revealing the different properties of the two flavonoids.
The aim of the present studies was to characterise cell death following inhibition of mitochondrial complex I with rotenone in a transformed cell line (RGC-5 cells) and to examine the neuroprotective ...properties of the flavonoids genistein, epigallocatechin gallate (EGCG), epicatechin (EC) and baicalin. Rotenone-induced cell death of RGC-5 cells results in a generation of reactive oxygen species, a breakdown of DNA, the translocation of membrane phosphatidylserine, an up-regulation of haemoxygenase-1 and is unaffected by necrostatin-1 (inhibitor of necroptosis), z-VAD-fmk (pan caspase inhibitor) or NU1025 (PARP inhibitor) but attenuated with SP600125 (JNK inhibitor). Rotenone-induced toxicity of RGC-5 cells also caused an activation of mitogen-activated kinases indicated by an up-regulation and translocation into mitochondria of p-c-Jun, pJNK and pp38. Exposure of RGC-5 cells to rotenone does not affect apoptosis inducing factor or significantly stimulate caspase-3 activity. EGCG and EC both significantly blunt rotenone toxicity of RGC-5 cells at concentrations of 50 μM while genistein and baicalin were without effect. Significantly, genistein is approximately 20 times less efficacious than EGCG (IC
50
2.5 μM) and EC (IC
50
1.5 μM) at inhibiting sodium nitroprusside-induced lipid peroxidation. These studies show that rotenone toxicity of RGC-5 cells is neither necroptosis nor caspase-dependent apoptosis but involves the activation of mitogen-activated kinases and is inhibited by a JNK inhibitor, EGCG and EC. Genistein attenuates lipid peroxidation less efficaciously than EC and EGCG and does not affect rotenone toxicity of RGC-5 cells.
The retina captures and converts light between 400–760 nm into electrical signals that are sent to the brain by way of the optic nerve and in the process helps to translate these electrical signals ...into what is known as vision. The same light that allows vision to occur is nevertheless also potentially toxic to retinal cells in certain situations. The shorter wavelengths of light are known to interact with chromophores in photoreceptors and pigment epithelial cells to cause oxidative stress and severe damage. Indeed it is generally accepted that short wavelength light effects is one cause for loss of photoreceptor function in age-related macular degeneration. Recent studies have demonstrated that light may be a contributing factor for the death of retinal ganglion cells in certain situations. Light as impinging on the retina, especially the short wavelength form, affect mitochondrial chromophores and can result in neurone death. Importantly ganglion cell axons within the eye are laden with mitochondria and unlike the outer retina are not protected from short wavelength light by macular pigments. It has therefore been proposed that when ganglion cell function is already compromised, as in glaucoma, then light impinging on their mitochondria might be a contributor to their eventual demise.
Deduce whether the isoflavone genistein blunts the effect of ischaemia to the retina.
Ischaemia was induced in rats by raising the intraocular pressure (120 mm Hg) for 50 min. Genistein (10 mg/kg) ...was injected intraperitoneally 1 h before and after ischaemia. Seven days after ischaemia, the level of mRNAs for neurofilament light (NF-L), caspase 3, caspase 8, glial fibrillary acidic protein (GFAP), poly-ADP ribose polymerase (PARP), Thy-1 and proteins (GFAP, NF-L, PARP) in whole retinas were determined. NF-L and tubulin proteins in optic nerves were also determined. Retinas were also processed for the localization of choline acetyltransferase (ChAT) and GFAP immunoreactivities.
Ischaemia caused a significant reduction in ganglion cell proteins in the optic nerve (NF-L and tubulin) and retina (NF-L). Retinal Thy-1 (mRNA and protein) and NF-L (mRNA) were also reduced while mRNAs of caspase 3, caspase 8, PARP and GFAP (also protein) were increased. Changes in the mRNAs and proteins induced by ischaemia were significantly blunted by genistein with the exception of the increase in GFAP and PARP protein/mRNA levels. Ischaemia-induced changes in the localization of ChAT were also clearly attenuated by genistein treatment.
Genistein blunts most of the damaging effects caused to the retina by ischaemia.
Orbital arteriovenous malformation is a rare condition which poses a management problem in view of the complexity of the vessels involved, and the potentially blinding and life-threatening ...complications from the modes of treatment. Treatment requires obliteration of the abnormal vascular communication. Vision may be adversely affected by the condition itself, as well as a result of invasive treatment modalities. This case reports such a situation where the visual outcome was severely affected following embolization of the feeding vessels.
Purpose To investigate the neuroprotective properties of three different flavonoids.
Methods : Immortalized retinal ganglion cells (RGC‐5 cells) in culture were exposed H2O2, rotenone or GB in the ...presence or absence of EG, EGCG or genistein and cultures analysed by viability assays, immunocytochemistry, western blot, stimulation of reactive oxygen species (ROS) and for histological evidence for apoptosis.
Results Insults of H2O2, rotenone and GB resulted in a time and dose‐dependent stimulation of ROS associated with an apoptotic type of cell death of RGC‐5 cells. Importantly, EG blunted these effects significantly but genistein was ineffective. In contrast, EGCG attenuated these affects only for insults induced by H2O2 and rotenone and not by GB.
Conclusion The results suggest the idea that defined insults can be attenuated by specific flavonoids.
Orbital arteriovenous malformation is a rare condition which poses a management problem in view of the complexity of the vessels involved, and the potentially blinding and life-threatening ...complications from the modes of treatment. Treatment requires obliteration of the abnormal vascular communication. Vision may be adversely affected by the condition itself, as well as a result of invasive treatment modalities. This case reports such a situation where the visual outcome was severely affected following embolization of the feeding vessels.
Numerous medical situations arises where the need for an accurate measurement of the volume of the orbital region in the human is required for further analysis/diagnosis. Various methods have been ...employed for this purpose. Computerised methods have had various limitations and effort is ongoing to further improve the results. Conventional approach would be to outline the shape on the two dimensional (2D) computed tomography (CT) and then to compute the volume slice by slice. This 2D approach allows for errors which can be improved using three dimensional (3D) geometrical theorems. As such, we propose a novel method using 3D geometrical techniques on a 3D virtual biomodel reconstructed from computed tomography (CT) scans of a patient which we term as Eye Orbital 3D Geometry Growth Algorithm (EOGGA). The method is described here together with preliminary results. The 2D method is also described and the comparison of the results agrees to each other. Effort is currently under way to elucidate the proposed method and to evaluate its utility in clinical treatment and surgical planning software.
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