A study on protective effects of epigallocatechin gallate on encephaledema following traumatic brain injury in rats / 中国中西医结合急救杂志

ABSTRACT

Objective To observe the inhibitory effect of epigallocatechin gallate (EGCG) on encephaledema following traumatic brain injury (TBI) in rats and its mechanism.Methods 200 Wistar rats were randomly divided into three groups: sham operation (n= 20), model (n= 90) and EGCG (n= 90) groups. The classic Feeney free fall drop method was used to establish the model of TBI. In EGCG group, intraperitoneal injection of EGCG in normal saline 100 mg/kg (10 mL/kg) was immediately given to the rats after model establishment, and in model group, equal amount of normal saline was administered with the same method, once 24 hours for 2 days in all the groups. At 24, 48, and 72 hours after the administration in various groups, the changes of water content, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level in brain tissues were determined, cerebral vascular permeability was evaluated by evans blue (EB) content in the brain tissues, the changes of expressions of aquaporin-4 (AQP4) and glial fibrillary acidic protein (GFAP) in brain tissues were determined by immunohistochemical and Western Blot, and the cerebral histopathological changes were observed in various groups.Results Compared with sham operation group, the water content, the vascular permeability and MDA level in brain tissues were significantly higher, while the cerebral SOD activity was significant lower in the model group; the scores of cells with positive AQP4 and GFAP expressions (IHC score) were obviously increased at 24 hours and 72 hours after model establishment, and the levels of expressions of AQP4 and GFAPprotein [integral absorbance (IA) value] were markedly enhanced in model group than those in the sham operation group, the changes being more remarkable at 72 hours after model formation [water content in brain tissues: (89.71±0.94)% vs. (78.34±0.87)%, EB content (μg/g): 9.13±0.66 vs. 2.71±0.72, SOD activity (U/mg): 63.53±12.57 vs. 130.85±9.91, MDA (nmol/mg): 10.19±1.47 vs. 4.57±0.74, IHC score of AQP4: 8.81±1.75 vs. 2.76±0.82, IHC score of GFAP: 9.47±1.32 vs. 6.71±0.52, expression of AQP4 protein (IA value): 1.53±0.05 vs. 0.42±0.05, expression of GFAP protein (IA value): 1.45±0.05 vs. 0.62±0.04, allP < 0.01]. Compared with the model group, the cerebral water content, MDA, IHC scores and protein expressions of AQP4 and GFAP, and cerebral vascular permeability were significantly decreased, while the SOD activity was obviously increased in the EGCG group, and the changes being more significant at 72 hours after model establishment [water content of brain tissues: (86.59±0.89)%, EB content (μg/g): 7.82±0.32, SOD activity (U/mg): 107.58±10.87, MDA (nmol/mg): 5.61±1.64, IHC score of AQP4: 6.92±0.71, IHC score of GFAP: 6.71±0.52, expression of AQP4 protein (IA value): 1.14±0.06, expression of GFAP protein (IA value): 1.21±0.07, all P < 0.01]. Imunohistochemical assay showed: the cerebral contents of AQP4 and GFAP positive cells in the rats of EGCG group were decreased, and their color became lighter.Conclusion The inhibition of EGCG on encephaledema following TBI in rats is related to its effects of decreasing the cerebral vascular permeability, enhancing the level of SOD activity, depressing MDA level and the expressions of AQP4 and GFAP.