Objective: We previously found that green tea catechins (GT-catechin) decrease oxidative damage to DNA and suppress brain dysfunction in aged senescence-accelerated mice (SAMP10). To clarify the effect of GT-catechin on suppression of brain dysfunction, we compare the effect on learning ability among several catechins and examined the essential intake period for prevention of brain dysfunction.
Methods: Male SAMP10 mice were allowed free access to water containing epigallocatechin gallate (EGCG, 0.06 mg/ml), epigallocatechin (EGC, 0.03 mg/ml), GT-catechin (0.2 mg/ml), or green tea extract (0.66 mg/ml). Learning ability of mice was measured using a step-through passive avoidance task.
Results: SAMP10 mice exhibit brain dysfunction with aging. However, learning ability was significantly higher in mice that drank GT-catechin and EGCG than same-aged control mice that drank water. EGCG was an important component, but EGC had no effect on learning ability. The learning ability was significantly improved in mice that ingested EGCG for > 5 months, and tended to improve in mice that ingested EGCG for 2 or 3 months. Next, the level of synaptophysin, a marker of presynapse, tended to be higher in mice that ingested EGCG but not in mice that ingested EGC. The levels of synaptophysin were significantly higher in mice ingested GT-catechin and green tea extract than control mice.
Conclusion: The intake of EGCG, the major catechin in green tea, but not EGC, suppressed age-related brain dysfunction. The effective intake period of EGCG was > 5 months for suppression of brain dysfunction.

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Objective: Advanced glycation end products (AGEs) accumulate in tissues due to aging, diabetic complications, and atherosclerosis. The acid lability of N^ω-carboxymethylarginine (CMA) present in glycated collagen has hampered detailed studies on its function and in vivo localization. In the present study, we analyzed the effects of collagen glycation on human dermal fibroblast (HDF) function. We also took advantage of Klotho-deficient mice (kkl/kl), which undergo accelerated senescence, to determine glycated collagen’s tissue localization.
Methods: Bovine type I collagen was incubated with ribose, and CMA formation was measured by enzyme-linked immunosorbent assay (ELISA). We measured the contraction of 3-dimensional matrix gels (3D gel), consisting of either native or glycated collagens, after culture with HDFs. CMA accumulation in Klotho-deficient mouse skin was measured by immunohistochemical staining.
Results: When collagen was incubated with ribose, CMA levels increased with time. In our HDF culture system, gels prepared with native, but not glycated collagen, contracted with time. In Klotho-deficient mice, CMA localized to the extracellular dermal matrix.
Conclusion: Here we show that CMA may provide a marker for collagen glycation, which may adversely affect HDFs’ growth and survival. Therefore, treatment with AGE inhibitors might help prevent pathologies associated with AGE formation.

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Chronic and repeated sun exposure causes photoaging skin that includes solar lentigines, wrinkles, changes of texture, benign tumors, and cutaneous cancers. Various symptoms of photoaging have been a great concern in dermatology. Photoprotection using sunscreens is recommended to prevent these signs. Two measures, sun protection factor (SPF) for UVB and protection grade of UVA (PA) for UVA, are described on the label of sunscreens. Our recent investigation revealed defects in the correct knowledge of SPF and PA and a relationship between freckles and sun-exposure history. Education in the appropriate use of sunscreens and the significance of SPF and PA is needed.
Solar lentigines on the face decrease quality of life. Previous laser therapies cause erosion and crusts with downtime for the treatment of pigmentary lesions. Then, intense pulsed light (IPL) sources have been developed as noninvasive and nonablative modalities for facial solar lentigines. We demonstrated clinical effectiveness of an IPL source for solar lentigines and ephelides on the face with well tolerability. Then, we performed a histopathological study that indicated IPL produced highly selective photothemolysis of melanin pigment in the lesions of solar lentigines, leading to the clinical improvement. Moreover, we showed clinical effects of a novel IPL source on solar lentigines and ephelides. In the future, phototherapy including IPL sources will develop with more effectiveness and safety.

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