The Effect of Trehalose Supplementation on Macrovascular Inflammation Biomarker in Old Rats by Assessing NFκB-p65 Expression
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Background: Vascular inflammation is one of contributing factors to the pathogenesis of arterial aging. Age-related activation of the inflammatory process can lead to various macro-and microvascular pathologies. The pro-inflammatory microenvironment generated in the vascular wall can lead to the pathogenesis of vascular diseases due to an increase in vascular dysfunction. Trehalose is a disaccharide that has several functions, protecting against stressors (one of them is reactive oxygen species/ROS) and preventing the inflammatory responses induced by endotoxic shock.
Objectives: To analyze the effect of trehalose supplementation on macrovascular inflammatory processes related to the aging process.
Methods: The experimental study used 28 male Wistar rats (Rattus novergicus) which were divided into 4 groups, young control group (Group A), old control group (Group B), 2% sucrose group (Group C), and 2% trehalose group (Group D); were then observed for 8 weeks.
Results: The results showed that there were no significant differences in aortic tissue NFκB-p65 expression between old and young subjects (p=0.247). The 2% trehalose group had 40% lower aortic tissue NFkB-p65 expression compared to the old control group (p=0.012); while the group given 2% sucrose solution had a 30% higher aortic tissue NFkB-p65 expression compared to the trehalose group (p=0.018).
Conclusion: Trehalose has a good effect on aging-associated vascular inflammatory processes that can be seen from the low aortic tissue NFκB-p65 expression in old rats.
American Heart Association, I. 2020 Heart Disease & Stroke Statistical Update Fact Sheet Global Burden of Disease. Am. Hear. Assoc. Inc 9–11 (2020).
Maharani, A. et al. Cardiovascular disease risk factor prevalence and estimated 10-year cardiovascular risk scores in Indonesia: The SMARThealth Extend study. PLoS One 14, 1–13 (2019).
Steven, S. et al. Vascular inflammation and oxidative stress: Major triggers for cardiovascular disease. Oxid. Med. Cell. Longev. 2019, (2019).
Kaplon, R. E. et al. Oral trehalose supplementation improves resistance artery endothelial function in healthy middle-aged and older adults. Aging (Albany. NY). 8, 1167–1183 (2016).
Echigo, R. et al. Trehalose treatment suppresses inflammation, oxidative stress, and vasospasm induced by experimental subarachnoid hemorrhage. J. Transl. Med. 10, 1–13 (2012).
Yoshizane, C. et al. Daily consumption of one teaspoon of trehalose can help maintain glucose homeostasis: A double-blind, randomized controlled trial conducted in healthy volunteers. Nutr. J. 19, 1–9 (2020).
Arai, C. et al. Trehalose prevents adipocyte hypertrophy and mitigates insulin resistance in mice with established obesity. J. Nutr. Sci. Vitaminol. (Tokyo). 59, 393–401 (2013).
Svenkrtova. Stratification of Yeast Cells during Chronological Aging by Size Points to the Role of Trehalose in Cell Vitality. 17, 395–408 (2017).
Seo, Y., Kingsley, S., Walker, G., Mondoux, M. A. & Tissenbaum, H. A. Metabolic shift from glycogen to trehalose promotes lifespan and healthspan in Caenorhabditis elegans. Proc. Natl. Acad. Sci. U. S. A. 115, E2791–E2800 (2018).
Sciarretta, S. et al. Trehalose-Induced Activation of Autophagy Improves Cardiac Remodeling After Myocardial Infarction. J. Am. Coll. Cardiol. 71, 1999–2010 (2018).
Berry, A. et al. Trehalose administration in C57BL/6N old mice affects healthspan improving
motor learning and brain anti-oxidant defences in a sex-dependent fashion: a pilot study. Exp. Gerontol. 129, 110755 (2020).
Nistiar, F. et al. Age dependency on some physiological and biochemical parameters of male Wistar rats in controlled environment. J. Environ. Sci. Heal. - Part A Toxic/Hazardous Subst. Environ. Eng. 47, 1224–1233 (2012).
Charalambous, M. P., Lightfoot, T., Speirs, V., Horgan, K. & Gooderham, N. J. Expression of cox-2, nf-κb-p65, nf-κb-p50 and ikkα in malignant and adjacent normal human colorectal tissue. Br. J. Cancer 101, 106–115 (2009).
Lee, S. J. & Park, S. H. Arterial aging. Korean Circ. J. 43, 73–79 (2013).
Lopez-candales, A., Burgos, P. M. H., Hernandez-Suarez, D. F. & Harris, D. Linking Chronic Inflammation with Cardiovascular Disease: From Normal Aging to the Metabolic Syndrome. 3, (2017).
Biwas, I. & Rezaie, A. R. Vascular inflammation in aging. 10, 3634–3635 (2018).
Ungvari, Z., Tarantini, S., Donato, A. J., Galvan, V. & Csiszar, A. Mechanism of Vascular Aging. Circ Res 123, 849–867 (2018).
Adi, A. M. Teknik Imunostaining. Bahan ajar (2013).
Janega, P. et al. Red wine extract decrease pro-inflammatory markers, nuclear factor-κB and inducible NOS, in experimental metabolic syndrome. Food Funct. 5, 2202–2207 (2014).
Fernández-Friera, L. et al. Vascular Inflammation in Subclinical Atherosclerosis Detected by Hybrid PET/MRI. J. Am. Coll. Cardiol. 73, 1371–1382 (2019).
Wissler, R. W. et al. Natural history of aortic and coronary atherosclerotic lesions in youth: Findings from the PDAY study. Arterioscler. Thromb. 13, 1291–1298 (1993).
Eikendal, A. L. M. et al. Relation between circulating inflammatory chemokines and vascular characteristics in healthy, young children. J. Am. Heart Assoc. 4, 1–10 (2015).
Sergin, I. et al. Exploiting macrophage autophagy-lysosomal biogenesis as a therapy for atherosclerosis. Nat. Commun. 8, 1–20 (2017).
Jayakumar, T. et al. Brazilin ameliorates high glucose-induced vascular inflammation via inhibiting ROS and CAMs production in human umbilical vein endothelial cells. Biomed Res. Int. 2014, (2014).
Blankstein, R., Libby, P. & Bhatt, D. L. Arterial Inflammation. 73, 10–12 (2019).
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