Antiaging Effects of Vicatia thibetica de Boiss Root Extract on Caenorhabditis elegans and Doxorubicin-Induced Premature Aging in Adult Mice.

The roots of Vicatia thibetica de Boiss are a kind of Chinese herb with homology of medicine and food. This is the first report showing the property of the extract of Vicatia thibetica de Boiss roots (HLB01) to extend the lifespan as well as promote the healthy parameters in Caenorhabditis elegans (C. elegans). For doxorubicin- (Doxo-) induced premature aging in adult mice, HLB01 counteracted the senescence-associated biomarkers, including P21 and γH2AX. Interestingly, HLB01 promoted the expression of collagen in C. elegans and mammalian cell systemically, which might be one of the essential factors to exert the antiaging effects. In addition, HLB01 was also found as a scavenger of free radicals, thereby performing the antioxidant ability. Lifespan extension by HLB01 was also dependent on DAF-16 and HSF-1 via oxidative stress resistance and heat stress resistance. Taken together, overall data suggested that HLB01 could extend the lifespan and healthspan of C. elegans and resist Doxo-induced senescence in mice via promoting the expression of collagen, antioxidant potential, and stress resistance.

Spectroscopic Signature of Red Blood Cells in a D-Galactose-Induced Accelerated Aging Model.

This work presents a semi-quantitative spectroscopic approach, including FTIR-ATR and Raman spectroscopies, for the biochemical analysis of red blood cells (RBCs) supported by the biochemical, morphological and rheological reference techniques. This multi-modal approach provided the description of the RBC alterations at the molecular level in a model of accelerated aging induced by administration of D-galactose (D-gal), in comparison to natural aging. Such an approach allowed to conclude that most age-related biochemical RBC membrane changes (a decrease in lipid unsaturation and the level of phospholipids, or an increase in acyl chain shortening) as well as alterations in the morphological parameters and RBC deformability are well reflected in the D-gal model of accelerated aging. Similarly, as in natural aging, a decrease in LDL level in blood plasma and no changes in the fraction of glucose, creatinine, total cholesterol, HDL, iron, or triglycerides were observed during the course of accelerated aging. Contrary to natural aging, the D-gal model led to an increase in cholesterol esters and the fraction of total esterified lipids in RBC membranes, and evoked significant changes in the secondary structure of the membrane proteins. Moreover, a significant decrease in the phosphorous level of blood plasma was specific for the D-gal model. On the other hand, natural aging induced stronger changes in the secondary structures of the proteins of the RBCs' interior. This work proves that research on the aging mechanism, especially in circulation-related diseases, should employ the D-gal model with caution. Nonetheless, the D-gal model enables to imitate age-related rheological alterations in RBCs, although they are partially derived from different changes observed in the RBC membrane at the molecular level.

Protective effects of ginsenoside Rg1 on splenocytes and thymocytes in an aging rat model induced by d-galactose.

Physiological aging is associated with a range of medical problems. However, the treatment of aging-associated diseases and prolonging human life are vital to our current aging societies. Panax ginseng, a traditional Chinese medicine, has been shown to have anti-oxidative and anti-aging effects. In the current study, aging rats induced by d-galactose were administered ginsenoside Rg1, then splenocytes and thymocytes were extracted and changes in activity were detected. The results demonstrated that compared with the d-gal group, the level of advanced glycation end products (AGE), the ratio of splenocytes and thymocytes in G0 phase (%), and apoptosis (%) of splenocytes and thymocytes, the ratio (%) of SA-gal positive splenocytes and thymocytes, the content of reactive oxygen species (ROS) and malondialdehyde (MDA), the ratio of glutathione (GSH) to oxidized glutathione (GSSG) and senescence-associated protein expression were significantly decreased and the index of the spleen and thymus, the proportion of white pulp in the spleen, the proportion of cortex in the thymus, the content of interleukin-2 (IL-2), interleukin-6 (IL-6), granulocyte-macrophage colony stimulating factor (GM-CSF), tumor necrosis factor-α (TNF-α), the activities of superoxide dismutase (SOD), and the proliferative capacity of splenocytes and thymocytes were increased in the Rg1+ d-gal group. These findings demonstrated that ginsenoside Rg1 may antagonize spleen and thymus damage in d-galactose-induced aging rats by alleviating oxidative stress injury and down-regulating the expression of senescence-associated protein.

Effect of Colla corii asini (E'jiao) on D-galactose induced aging mice.

Colla corii asini (E'jiao), donkey-hide gelatin prepared by stewing and concentrating from Equus asinus L. donkey hide, is a traditional Chinese medicine preparation widely used in clinical hematic antanemic therapy in China. The aim of the present study was to investigate potential anti-aging effect of Colla corii asini and explore related mechanisms in D-galactose (gal) induced aging model mice. The mice were artificially induced aging by subcutaneously injection with D-gal at the dose of 100 mg/kg·d for 8 weeks. Colla corii asini was simultaneously treated to them once daily by intragastric gavage. Appetite, mental condition, body weight, and organ index were observed. Activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), as well as levels of malondialdehyde (MDA) in serum, brain, and liver were determined by according assay kits. Western blotting analysis was used to detect p16 and p21 expression. Results indicated that Colla corii asini could improve appetite, mental condition, body weight, and organ condition of model mice, improve SOD, CAT, and GSH-Px activities, reduce MDA levels, and modulate age-related genes expression in D-gal induced mice. Therefore, Colla corii asini may have effect to suppress the aging process through enhancing antioxidant activity, scavenging free radicals, and modulating aging-related gene expression.

Neuroprotective effect of hydroalcoholic extract of dried fruits of Trapa bispinosa Roxb on lipofuscinogenesis and fluorescence product in brain of D-galactose induced ageing accelerated mice.

Effect of hydroalcoholic extract T. bispinosa (TB) was studied on fluorescence product and biochemical parameter like lipid peroxidation, catalase activity and glutathione peroxidase activity in the brain of female albino mice. Ageing was accelerated by the treatment of 0.5 ml 5% D-galactose for 15 days. This resulted in increased fluorescence product, increase lipid peroxidation and decrease antioxidant enzyme like glutathione peroxides and catalase in cerebral cortex. After cotreatment with hydroalcoholic extract of TB (500 mg/kg, po) there was decrease in fluorescence product in cerebral cortex. Moreover, TB inhibited increase lipid peroxidation and restores glutathione peroxidase and catalase activity in cerebral cortex as compare to ageing accelerated control group. To conclude TB found to be effective antioxidative agent which could to some extent reverse D-galactose induced ageing changes resulted due to oxidative damage.

Protective role of salidroside against aging in a mouse model induced by D-galactose.

OBJECTIVE: To investigate the protective effects of putative AGEs (advanced glycation endproducts) inhibitor salidroside against aging in an accelerated mouse aging model induced by D-galactose. METHODS: A group of 5-month-old C57BL/6J mice were treated daily with D-galactose, D-galactose combined with salidroside, salidroside alone, and control buffer for 8 weeks. At the end of the treatment, serum AGEs levels, neurological activities, expression of glial fibrillary acidic protein (GFAP) and neurotrophin-3 (NT-3) in the cerebral cortex, as well as lymphocyte proliferation and IL-2 production were determined. RESULTS: D-galactose induced mouse aging model was developed as described before. As expected, salidroside blocked D-galactose induced increase of serum AGEs levels. It also reversed D-galactose induced aging effects in neural and immune system, as evidenced by improving motor activity, increasing memory latency time, and enhancing lymphocyte mitogenesis and interleukin-2 (IL-2) production. Furthermore, elevated expression of GFAP and NT-3 in the aged model mice was also reduced upon salidroside treatment. CONCLUSION: Salidroside inhibits AGEs formation in vivo, which at least partially contributes to its anti-aging effect in D-galactose induced aging model.

Contributions of DNA interstrand cross-links to aging of cells and organisms.

Impaired DNA damage repair, especially deficient transcription-coupled nucleotide excision repair, leads to segmental progeroid syndromes in human patients as well as in rodent models. Furthermore, DNA double-strand break signalling has been pinpointed as a key inducer of cellular senescence. Several recent findings suggest that another DNA repair pathway, interstrand cross-link (ICL) repair, might also contribute to cell and organism aging. Therefore, we summarize and discuss here that (i) systemic administration of anti-cancer chemotherapeutics, in many cases DNA cross-linking drugs, induces premature progeroid frailty in long-term survivors; (ii) that ICL-inducing 8-methoxy-psoralen/UVA phototherapy leads to signs of premature skin aging as prominent long-term side effect and (iii) that mutated factors involved in ICL repair like ERCC1/XPF, the Fanconi anaemia proteins, WRN and SNEV lead to reduced replicative life span in vitro and segmental progeroid syndromes in vivo. However, since ICL-inducing drugs cause damage different from ICL and since all currently known ICL repair factors work in more than one pathway, further work will be needed to dissect the actual contribution of ICL damage to aging.