2020
DOI: 10.1080/13813455.2020.1838550
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The effects of melatonin against atherosclerosis-induced endothelial dysfunction and inflammation in hypercholesterolemic rats

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Cited by 11 publications
(3 citation statements)
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“…The result of our study is different from that reported by Ismail and Mahmood (2022) who found that there was a highly significant difference and variability bout changes in lipid profiles in melatonin group than without melatonin group and this difference may be due to that this study was shorter than our study, and further they used streptozotocin-induced rat while we used atherosclerosis induced rabbits [14]. Furthermore, it has recently been discovered that while melatonin has no effect on total cholesterol, it greatly increases the serum triglyceride and HDL-C level [15,16].…”
Section: Resultsmentioning
confidence: 59%
“…The result of our study is different from that reported by Ismail and Mahmood (2022) who found that there was a highly significant difference and variability bout changes in lipid profiles in melatonin group than without melatonin group and this difference may be due to that this study was shorter than our study, and further they used streptozotocin-induced rat while we used atherosclerosis induced rabbits [14]. Furthermore, it has recently been discovered that while melatonin has no effect on total cholesterol, it greatly increases the serum triglyceride and HDL-C level [15,16].…”
Section: Resultsmentioning
confidence: 59%
“…Melatonin has been shown to ameliorate ED in animal models of hypercholesterolemia and DM by regulating NO availability and inflammatory pathways; 18 , 19 , 20 however, clinical trials results are inconsistent in this regard. In a randomized clinical trial, 1 month of 10 mg oral melatonin was found to reduce serum markers of ED and increase serum NO levels in patients with severe CAD.…”
Section: Discussionmentioning
confidence: 99%
“…MAPK signaling pathways (Zhang J. et al, 2020). Melatonin may have protective and therapeutic effects on hypercholesterolemia by regulating vaspin, STAT-3, DDAH, and ADMA signaling pathways (Sezgin et al, 2020). Increased levels of STAT-1 promote SMC (Smooth muscle cell) de-differentiation, whereas high levels of STAT-3 drive SMC into a more mature phenotype (Kirchmer et al, 2014).…”
Section: Jak/stat Pathway In Oncopathologymentioning
confidence: 99%