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Nano Resveratrol: A Promising Future Nanonutraceutical
Published in Bhupinder Singh, Minna Hakkarainen, Kamalinder K. Singh, NanoNutraceuticals, 2019
Chahinez Houacine, Kamalinder K. Singh
Substantial investigations have been carried out to increase longevity and improve the lifespan. On exploration of various model organisms including fruit flies, yeast, and rodents, it is found that resveratrol triggers genes linked with longevity, especially a class of genes, known as sirtuins, which enhance the survival. It is the strongest activator of SIRT1, which acts in the same way as the pathways induced by caloric restriction, thus preventing chronic diseases and increasing the lifespan. Resveratrol’s mechanisms of action are quite complex, with a plethora of effects in various tissues. The effects are frequently dependent on the physiologic status of the cells, for example, normal cells vs. specific cancer cell lines vs. cells with oxidative damage.
Herbal Therapies
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
H. Shahrul, M. L. Tan, A. H. Auni, S. R. Nur, S. M. N. Nurul
Berberine is an alkaloid with pharmacological effects (Neag et al., 2018). Berberine is found in numerous herbs; however, the major natural source of berberine is derived from Berberis. Alkaloid content in its bark is more than 8% with berberine as main alkaloid (Arayne et al., 2007; Imanshahidi and Hosseinzadeh, 2008). Plants rich with berberine content are used traditionally worldwide for healing ailments. Interestingly, its cardiovascular protective role includes hypotensive effects, inotropic, anti-inflammatory effects, dilation of coronary artery, anticoagulation, lowering pulse, and lowering of elevated low-density lipoprotein cholesterol (Neag et al., 2018). As a cardioprotective compound, berberine up-regulates endothelial nitric oxide synthase (eNOS) mRNA expression. It also increases production of nitric oxide (NO) from arginine. This is facilitated by the activity of eNOS. It is reported to play an important role in vasodilation (Wang et al., 2009). NO mediates the endothelium-dependent relaxation in large conduit arteries. Abnormal production of NO would cause vascular and endothelial dysfunction (Furchgott, 1999; Tawfik et al., 2006). Apart from that, the accumulation of lipid-laden foam cells initiates the progression of atherosclerosis because of augmented inflammation and impaired cholesterol metabolism within vascular walls. Berberine’s anti-atherogenic effects are manifested by suppression of ox-LDL-induced foam cell growth and cholesterol accumulation in macrophages by regulation of surtuin 1 (SIRT1) and peroxisome proliferator-activated receptor-γ (PPAR-γ) (Chi et al., 2014). Accumulation of fatty acid is reduced by SIRT1. It would repress PPAR-γ which is involved in atherogenesis (Picard et al., 2004). Overexpression of SIRT1 could hinder atherosclerosis by improving vascular function (Zhang et al., 2008b).
Selenomethionine attenuates D-galactose-induced cognitive deficits by suppressing oxidative stress and neuroinflammation in aging mouse model
Published in Gary Bañuelos, Zhi-Qing Lin, Dongli Liang, Xue-bin Yin, Selenium Research for Environment and Human Health: Perspectives, Technologies and Advancements, 2019
J.J. Wang, X.X. Liu, Z.D. Zhang, Q. Zhang, C.Y. Wei*
SIRT1 deacetylase for numerous proteins is involved in several cellular pathways, including stress response and apoptosis, and plays a protective role in neurodegenerative disorders (Godoy et al. 2014). It has been involved in the regulation of signal transduction cascades associated with NF-kB pathways (Fougère et al. 2016). The decreased expression of SIRT1 and PPARγ in D-gal-treated mice is evidenced as described above.
Higher sirt1 is associated with a better body composition in master sprinters and untrained peers
Published in European Journal of Sport Science, 2023
Patrício Lopes de Araújo Leite, Larissa Alves Maciel, Patrick Anderson Santos, Lucas Pinheiro Barbosa, Sara Duarte Gutierrez, Hugo de Luca Corrêa, Lysleine Alves de Deus, Marcia Cristina Araújo, Samuel da Silva Aguiar, Thiago dos Santos Rosa, John E. Lewis, Herbert Gustavo Simões
Another important finding of the current study was that MS showed attenuation of the usual age-related decline in Sirt1. Lifelong exercise seems to preserve Sirt1 for master athletes, which in turn may be related to attenuated biological aging, given that telomere length is maintained in this population (Aguiar et al., 2021; Simoes et al., 2017). Other studies have shown the importance of exercise training in increasing circulating levels of Sirt (Aguiar et al., 2022; Pucci et al., 2013; Vargas-Ortiz et al., 2019). Some mechanisms have been proposed to explain the activation of Sirt through exercise. Exercise training depends on a continuous supply of energy for muscle performance, which can be provided through increased levels of NAD+, leading to the activation of the deacetylation mechanism of Sirt1. This last process may in turn lead to mitochondrial biogenesis and improved oxidative capacity through the pathway of PGC-1α. Thus, increased NAD may be pivotal (Pucci et al., 2013; Vargas-Ortiz et al., 2019).
Protective and curative role of Spirulina platensis extracts on cisplatin induce acute kidney injury in rats
Published in Egyptian Journal of Basic and Applied Sciences, 2019
Mahmoud M. Zakaria, Fatma Mohamed Mansour El-Tantawy, Sherry Mohamed Khater, Safaa A. Derbala, Verginia Mohamed El-Metwally Farag, Abdel-Aziz Fatouh Abdel-Aziz
In the present study, it was found that the mean values of red blood cells, hemoglobin, white blood cells, platelets, MCV, MCH and MCHC, were significantly decreased in rats receiving Cp. Also, no significant differences in all hematological parameters in healthy rats receiving Sp were found when compared to a healthy control group. The anemia found in Cp-treated rats might be of the type caused by chronic disease; however, other causes include autoimmune hemolytic anemia, iron deficiency anemia, anemia of chronic renal failure and Cp myelotoxicity. Thrombocytopenia occurred in Cp-treated rats and it is a part of a broader hematological disturbance. All these disturbances in hematological parameters were improved in Sp-treated rats in comparison to their corresponding values in Cp-treated rat. These findings are in agreement with the result of another researcher who reported that disturbance in hematological parameter were more minimized if Sp was given before Cp and this indicates that Sp may have a great role deal with the process of erythropoiesis [41]. The present study found that, Cp administration induced elevation of Bax gene expression in kidney tissues, and this result was similar to those demonstrated by other researchers who indicated that the ratio of Bax/Bcl-2 protein expression in kidney tissues was increased following cisplatin injection. Indeed, the increase ratio of pro-apoptotic protein, Bax, and antiapoptotic protein, Bcl-2, determines the potential of cells to apoptosis process [42,43]. It is clear that Sp may be attenuated Cp effect and down regulated the pro-apoptotic protein (Bax) and this effect may be by up regulated the antiapoptotic protein (Bcl-2) corresponded with reduced apoptosis and improved renal function and this suggest a correlation between the changes in the mitochondrial pathway of apoptosis and the administration of Spirulina. Importantly, when the Bax gene was deleted, the animals became resistant to cisplatin and this illustrated that spirulina administration caused a protective effect on kidney or increased the antiapoptotic gene and decreasing the Bax apoptotic gene. In our experimental study, it is found that overexpression of Sirtuin 1 (SIRT1) in spirulina pre- and post-treatment has a significant protective effect against cisplatin-induced AKI. Actually, SIRT1 gene activation exerted cytoprotective effects through several mechanisms, including antiapoptosis, antioxidative and anti-inflammatory responses as well as the regulation of mitochondrial biogenesis, autophagy and metabolism in response to cellular energy and redox status [44]. SIRT1 deacetylates p53 and in turn decreases apoptosis through deacetylation of p53 inhibition. P53 may also increase the survival of the cancer cells and thus reduce the therapeutic efficiency of cisplatin [45,46]. Thus, spirulina exerts cytoprotective effects through SIRT1 activation.
The potential interaction of environmental pollutants and circadian rhythm regulations that may cause leukemia
Published in Critical Reviews in Environmental Science and Technology, 2022
Francisco Alejandro Lagunas-Rangel, Błażej Kudłak, Wen Liu, Michael J. Williams, Helgi B. Schiöth
Samples collected from AML patients showed downregulation of BMAL1, PER1, PER2, PER3, CRY1 and CRY2 (Table 1) that were negatively correlated with the amount of blast cells in the bone marrow and, therefore, indicate that in this type of cancer these proteins act as tumor suppressors (M.-Y. Yang et al., 2015). The downregulation of circadian clock genes in patients with AML was maintained until the end of treatment and those who relapsed showed an increase in CRY2 expression (Rahman et al., 2017). Related to this, increased DNA methylation of the PER3 promoter, an epigenetic mechanism of gene silencing, was observed in patients with AML and, as treatment with decitabine progressed, this methylation decreased and the expression levels of PER3 increased in patients with complete remission, while in those who relapsed, levels remained low (Y. Wang et al., 2011). The same pattern was observed in patients with complete remission and in those who relapsed for PER1 expression (M.-Y. Yang et al., 2015). In myeloid leukemic cells that possess the MLL-AF9 fusion gene, a marker associated with an intermediate to good prognosis, it was observed that down-regulation of the CLOCK and BMAL1 genes decreases their cell proliferation, induces their differentiation, and depletes the number of leukemic stem cells (LSCs) (Puram et al., 2016; Winters & Bernt, 2017). Contrastingly, although normal hematopoietic stem and progenitor cells (HSPCs) are also influenced by the circadian cycle, BMAL1 was not shown to be necessary for their self-renewal, differentiation, or multilineage engagement (Puram et al., 2016). To explain these differences, we must mention that oscillating levels of NAD + have been reported to control acetylation of histone methyltransferase mixed-lineage leukemia 1 (MLL1) (also known as histone-lysine N-methyltransferase 2 A (KMT2A)) via NAD+-dependent deacetylase SIRT1 (also called sirtuin 1) and, in turn, CLOCK-BMAL1-dependent transcriptional activation. When NAD + levels are low (e.g. nutrients high), MLL1 is acetylated and its activity increases causing high levels of H3K4me3 and high expression of CCGs, but when NAD + levels increase (e.g. nutrients low), SIRT1 deacetylates MLL1 and reduces its enzymatic activity leading to a decrease in H3K4me3 levels and in the expression of CCGs (Aguilar-Arnal et al., 2015). Then, MLL1 controls the levels of H3K4me3 and influences the levels of H3K9ac and H3K14ac in such a way that these have circadian oscillations in the CCG promoters. Also, MLL1 interacts, synergizes and is required for the proper recruitment of the CLOCK-BMAL1 dimer and the activation of CCG transcription (Katada & Sassone-Corsi, 2010). Thus, although low levels of BMAL1 are produced in normal cells, the presence of the normal and functional MLL1 protein that synergizes its transcriptional activation functions in CCGs promotes compensation against loss, while in leukemic cells, which express the MLL-AF9 fusion protein, where MLL1 loses several domains, including transactivation and histone methyltranferase SET domains, there is no way to compensate for the low levels of BMAL1.