Accumulating evidence suggests that yoga promotes a healthy life expectancy in humans; however, the molecular basis of this effect is not clear. Moderate exercise is known to activate sirtuin family genes by improving blood circulation and prevent aging. Hot yoga might have a particularly strong benefit to activate these sirtuin family genes, because prolonged exposure to high temperatures coupled with high humidity can increase blood flow. Here, we investigated the impact of hot yoga on characteristic features of aging by assessing body composition and blood biochemistry indexes in 48 healthy female volunteers (aged 20 to 59 years) before and after completion of a hot yoga program consisting of two 60 minutes lessons per week for 12 weeks. SIRT6 expression was increased and ROS levels were decreased in volunteers after completing the hot yoga program compared with before starting. Furthermore, we demonstrated that completion of the hot yoga program increased the moisture content in the stratum corneum and elasticity and improved skin texture. These results suggest that hot yoga can have a positive impact on various features associated with aging, suggesting that it might be useful in delaying senescence.

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Related to the great importance of the intra-arterial perivascular drainage (IPAD), the drainage function of the lipoprotein receptor-related protein-1 (LRP1) that is a huge transmembrane LRP receptor member, is increasingly becoming the subject of comprehensive researches. Two important questions thus emerged: 1. How does the binding of the whole ligand complex members, among them amyloid beta (Aβ), the crucial factor in the pathology and pathophysiology of Alzheimer's disease (AD), lead to conformational changes in the extracellular receptor structure? 2. How do these changes reflect in the structure of the receptor intracellular tail, with the binding of PICALM (phosphatidylinositol binding clathrin assembly protein) to the YXXL tail motif, and how do they reflect in the recruitment of a number of signal proteins, and in the onset of PICALM/clathrin Aβ endocytosis, transcytosis and Aβ exocytosis into the capillary circulation? Both questions require an exact explanation. The profound insight into the available literature related to these events does not give a satisfactory explanation to these questions; consequently, the present knowledge of the AD pathophysiology requires additional comprehensive research. This study is not concerned with the details of the AD pathology and pathophysiology; it is primarily concerned with the problem of Aβ binding to the LRP1, with local conformational changes in the tail, and with the activators of Aβ transcytosis and Aβ exocytosis into the capillary blood.

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Objectives: It has been reported that hair glycated over time from the root to the tip exhibits changes in physical properties, such as a decrease in breaking strength. However, few studies have examined the inhibition of hair glycation. In this study, we examined the anti-glycation effect of plant extracts to identify materials that inhibit hair glycation. Methods: A total of 26 plant extracts were used as the cosmetic ingredients. A glycation solution was prepared with 0.1 mol/L phosphate buffer (PB; pH 7.4), 5.0 mol/L glucose, and 5.0 mg/mL keratin; the sample to be tested was then added to this solution. After thermal reaction, the levels of advanced glycation end products (AGEs) produced in the reaction solution were measured using the fluorescence method (excitation wavelength 370 nm / detection wavelength 440 nm), and the AGE production inhibitory rate was calculated. In the primary screening, each sample was adjusted to a final concentration of 0.1 mg/mL in the reaction solution with deionized water, and the AGE production inhibition rate was measured. In the secondary screening, half maximal inhibitory concentration (IC50) was calculated and evaluated for samples with an AGE production inhibition rate of 75% or more obtained in the primary screening. Next, we obtained hair samples from healthy women in their 30s who had no history of beauty treatment, and verified the anti-glycation effects of the plant extracts. To verify the anti-glycation effect, the hair sample was immersed in 0.1 mol/L phosphate buffer (pH 7.4) containing 1.2 mol/L of glucose and 0.1 mg/mL of each sample, and reacted at 50°C for 10 days. Hair protein was extracted, and the levels of fluorescent AGEs were measured. The physical properties of the hair were measured using a tensile tester at ambient temperature (25°C) and humidity (65% RH). Results: Following primary screening, 75% or more of the AGE production inhibitory effect was observed in 9 out of 26 samples. The secondary screening results showed that the IC50 of rooibos extract had a stronger anti-glycation effect than the IC50 of aminoguanidine. An in vitro hair test showed that rooibos extract inhibited the production of fluorescent AGEs (production inhibition rate 82.4%). In addition, the breaking strength of the glycated hair was reduced by 20.8% compared to that of the un-glycated hair; however, after treatment with the rooibos extract, the reduction in breaking strength due to glycation could be suppressed to 4.9%. Conclusion: Rooibos extract was found to have an inhibitory effect on the production of fluorescent AGEs in hair proteins. It also showed an inhibitory effect on the decrease in the breaking strength of the hair due to glycation. These results indicate that the addition of rooibos extract to hair cosmetics may help inhibit the changes in the physical properties of hair caused by glycation.

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Accumulation of advanced glycation endproducts (AGEs) in the body due to glycative stress is a factor in the onset of aging and lifestyle-related diseases. Suppression of glycative stress is called anti-glycation. Anti-glycation includes suppression of postprandial hyperglycemia, suppression of glycation reaction, and decomposition and excretion of AGEs. Since aminoguanidine (AG), a substance having an AGE production inhibitory effect, has side effects, functional foods having a glycation reaction inhibitory activity are desired. In this study, for evaluating the anti-glycation effect of gardenia (Gardenia jasminoides Ellis) extract on the skin proteins, the glycation reaction inhibitory activity and AGE cross-linking breaking activity of genipin and crocetin, purified from gardenia, was measured. Keratin, collagen, and elastin were used as model proteins for the glycation reaction. Genipin and crocetin were found to suppress the production of fluorescent AGEs (F-AGEs), pentosidine, Nε-carboxymethyllysine (CML) and 3-deoxyglucosone (3DG). The activity of genipin on F-AGEs was strong with the half maximal inhibitory concentration (IC50) lower than that of crocetin. Its IC50 was 2.4 to 31.6 times lower than that of AG, a positive control. The AGE cross-linking breaking activity was 2.8 times stronger with genipin than with crocetin. These findings indicate that application of a preparation containing genipin and crocetin to the skin may improve the skin condition by suppressing the AGE production from skin proteins and by breaking the AGE cross-linking.

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