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Objective:To evaluate the skin development and repair process of X-ray radiation damage in rat with non-invasive two-photon excitation fluorescence (TPEF) imaging technology in vivo. Methods:Totally 24 SD rats were randomly divided into four groups including X-ray irradiated group (25, 35 and 45 Gy) and non-irradiation control group. At different times after irradiation, the degree of skin injury was evaluated, and the pathological changes of nicotinamide adenine dinucleotide (phosphate) [NAD(P)H] and collagen fiber fluorescence signals in epidermal cells were detected in vivo by TPEF imaging technology. Results:At 10 d post-irradiation, the skin of irradiation groups showed erythema and desquamation. At 15-20 d post-irradiation, the skin of radiation groups developed progressive exudation, edema and ulcers with increasing radiation dose. On day 25, the skin began to repair in the 25 Gy group, however, the skin of other groups still had exudation and ulcers. On day 10, NAD(P)H fluorescence signal in epidermal cells of irradiation groups decreased and the fluorescence signal of collagen fibers in papillary layer and reticular layer of irradiation groups reduced, which were significantly lower than that of normal control group ( t=24.145, 28.303, 26.989, 6.654, 7.510, 7.997, P<0.05). On day 30, fluorescence signal of NAD(P)H and collagen fibers in epidermal cells and dermis began to repair, the cell from stratum granulosum, stratum spinosum, and stratum basale in the 25 Gy group showed fluorescence signal, the other groups did not show. The fluorescence signal of collagen fibers in the 25 Gy group were gradually increased in papillary layer and reticular layer, however, they were significantly lower than normal control group ( t=115.133, 17.431, P<0.05), the skin of 45 Gy group did not show fluorescence signal of collagen fibers. Conclusions:The damage and repair process of epidermal cells and dermal collagen fiber can be detected noninvasively by TPEF imaging technology after X-ray irradiation in vivo.
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Objective To evaluate the efficiency of Ginkgo biloba extract 50 (GBE50) on learning memory ability and inflammatory response in hippocampus of natural aging mice, and explore the underlying anti-aging mechanisms.Methods 16-month-old ICR mice were randomly divided into three groups:model group, GBE50 low and high dose groups. 1 month mice were as normal group. The mice in GBE50 low and high dose groups received GBE50. The mice in the normal and model groups received solvent (1%CMC-Na+) by intragastric administration. The Morris water maze test and step-down test were used to assess behaviors of the mice. Immunofluorescent staining was used to detect the number of Iba-1 positive cells. The enzyme linked immunosorbent assay was used to determine the expression of TNF-α and IL-1β.Results Compared with normal group, escape latency and swimming distance in the Morris water maze test in the model group increased (P<0.05);latency shorted and error times decreased in the step-down test (P<0.05);the number of Iba-1 positive cell in the hippocampus CA1 in the model group increased considerably (P<0.01);TNF-α expression was in a general upward trend while IL-1β increased apparently (P<0.01). Compared with model group, escape latency and swimming distance decreased in the Morris water maze test in GBE50 high dose group;latency and the error times increased in the step-down test (P<0.05);the number of Iba-1 positive cells decreased (P<0.05). TNF-α expression showed a downward trend and IL-1β expression decreased in GBE50 low dose group (P<0.05). Conclusion GBE50 can delay aging and increase learning memory of natural aging mice.
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<p><b>OBJECTIVE</b>To investigate the regulating effect of Ginkgo biloba extract 50 (GBE50) on pre-inflammatory factors interleukin-1 beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and anti-inflammatory factors interleukin-4 (IL-4), interleukin-10 (IL-10) of hippocampus in senile rats, in order to explore the protective mechanism of GBE50 on central nervous system of senile animals.</p><p><b>METHOD</b>SD rats were randomly divided into four groups: the normal group, the model group, the GBE50 group and the EGB761 group. Rats were intraperitoneally injected with 100 mg x kg(-1) D-galactose every day for 42 days to establish the senile rat model. At the 21st day, the GBE50 group and the EGB761 group were orally administered with 60 mg x kg(-1) for 21 days. IL-1beta mRNA and TNF-alpha mRNA expressions were detected by real-time fluorescence quantitative PCR assay, IL-1beta and TNF-alpha protein expressions were detected by immunohistochemistry, IL-4 and IL-10 protein contents were detected by ELISA.</p><p><b>RESULT</b>D-galactose caused imbalance between pre-inflammatory factors and anti-inflammatory factors of hippocampus in senile rats, GBE50 and EGB761 reduced IL-1beta mRNA expression (P < 0.05) and TNF-alpha and IL-1beta protein level (P < 0.01) and up-regulated IL-10 protein content (P < 0.01, P < 0.05).</p><p><b>CONCLUSION</b>The mechanism of GBE50 in protecting central nervous system is probably related to its effect in mitigating inflammatory of central nervous system.</p>