Effects of Tongluo Recipe on oxidative stress and ultrastructure of hippocampus in Streptozotocin-induced diabetic rats
Liu Zhi-mi
Abstract
Liu Zhi-mi
Abstract
Objective To investigate the effects of Tongluo Recipe(TLR) on oxidative stress and ultrastructure of the hippocampus in streptozotocin-induced diabetic rats. Methods Diabetes was induced by a single intraperitoneal injection of streptozotocin ( 60 mg/kg) dissolved in citrate buffer. The streptozotocin-injected rats with blood glucose levels ≥16.7 mmol/L 3 days after injection were included in the study and were randomly divided into two groups:an untreated diabetic group and TLR treatment group. Rats in TLR treatment group received 0.4 g·kg-1·d-1 TLR treatment throughout the experiment. Rats in the untreated diabetic group and normal control group were given gastric perfusion of distilled water once at the same time and dose. After 12 weeks of treatment,superoxide dismutase (SOD),glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were measured in hippocampal tissues and plasma. The cellular ultrastructure of neurons in the hippocampus was observed through transmission electronic microscope. Results MDA levels were increased,GSH-Px and SOD activities were decreased in the plasma (P0.001) and hippocampus (P0.01) of untreated diabetic group compared to the controls. In untreated diabetic group,conspicuous intracytoplasmic vacuole formation was present in neurons in diabetic rat hippocampus; mitochondriales crista disappeared,some ribosomal particles became diffusely dispersed,and the nucleus became shrunken. TLR obviously ameliorated the morphological changes and improved SOD and GSH-Px activity. In TLR treatment group,the levels of GSH-Px and SOD were significantly increased and the levels of MDA were decreased in the plasma (P0.001) and hippocampus (P0.05) compared to those of the diabetic rats. Conclusion TLR can improve the ultrastructure and oxidative stress level,probably through depleting free radical production and increasing activities of antioxidatant.
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Objective To investigate the effects of Tongluo Recipe(TLR) on oxidative stress and ultrastructure of the hippocampus in streptozotocin-induced diabetic rats. Methods Diabetes was induced by a single intraperitoneal injection of streptozotocin ( 60 mg/kg) dissolved in citrate buffer. The streptozotocin-injected rats with blood glucose levels ≥16.7 mmol/L 3 days after injection were included in the study and were randomly divided into two groups:an untreated diabetic group and TLR treatment group. Rats in TLR treatment group received 0.4 g·kg-1·d-1 TLR treatment throughout the experiment. Rats in the untreated diabetic group and normal control group were given gastric perfusion of distilled water once at the same time and dose. After 12 weeks of treatment,superoxide dismutase (SOD),glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were measured in hippocampal tissues and plasma. The cellular ultrastructure of neurons in the hippocampus was observed through transmission electronic microscope. Results MDA levels were increased,GSH-Px and SOD activities were decreased in the plasma (P0.001) and hippocampus (P0.01) of untreated diabetic group compared to the controls. In untreated diabetic group,conspicuous intracytoplasmic vacuole formation was present in neurons in diabetic rat hippocampus; mitochondriales crista disappeared,some ribosomal particles became diffusely dispersed,and the nucleus became shrunken. TLR obviously ameliorated the morphological changes and improved SOD and GSH-Px activity. In TLR treatment group,the levels of GSH-Px and SOD were significantly increased and the levels of MDA were decreased in the plasma (P0.001) and hippocampus (P0.05) compared to those of the diabetic rats. Conclusion TLR can improve the ultrastructure and oxidative stress level,probably through depleting free radical production and increasing activities of antioxidatant.
Key concepts: Streptozotocin, Malondialdehyde, Oxidative stress, Internal medicine, Hippocampus, Endocrinology, Medicine, Superoxide dismutase