2013
DOI: 10.1016/j.fitote.2013.09.001
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Ginsenoside Rg1 exerts synergistic anti-inflammatory effects with low doses of glucocorticoids in vitro

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Cited by 37 publications
(15 citation statements)
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“…In addition, these models do not consider the possibility that adaptogens modulate receptor expression via other mechanisms. However, adaptogens exhibit multitarget action and the shared use of a number of different receptors, including receptors for corticosteroid, mineralocorticoid, progestin, estrogen, serotonin (5‐HT), N ‐methyl‐ d ‐aspartate, and nicotinic acetylcholine, receptor tyrosine kinases, and many G protein–coupled receptors . Therefore, the possibility that numerous molecular network interactions (with feedback regulation of the neuroendocrine and immune systems) contribute to the overall pharmacological response and result in agonist‐dependent antagonism is most suitable for understanding the mechanisms of action of adaptogens.…”
Section: Introductionmentioning
confidence: 99%
“…In addition, these models do not consider the possibility that adaptogens modulate receptor expression via other mechanisms. However, adaptogens exhibit multitarget action and the shared use of a number of different receptors, including receptors for corticosteroid, mineralocorticoid, progestin, estrogen, serotonin (5‐HT), N ‐methyl‐ d ‐aspartate, and nicotinic acetylcholine, receptor tyrosine kinases, and many G protein–coupled receptors . Therefore, the possibility that numerous molecular network interactions (with feedback regulation of the neuroendocrine and immune systems) contribute to the overall pharmacological response and result in agonist‐dependent antagonism is most suitable for understanding the mechanisms of action of adaptogens.…”
Section: Introductionmentioning
confidence: 99%
“…Except for NO, also the other pro-inflammatory cytokines (TNF-α and IL-1β) are over-produced in response to inflammatory stimuli and they also could induce an inflammation [17]. TNF-α is another major mediator in pro-inflammatory processes and produced in many types of cells, such as macrophages, monocytes and lymphocytes, in response to inflammation, infection, and other environmental challenges in host [28]. Though TNF-α is also a critical modulator of the hosts immune response to infection, over-production of TNF-α can be harmful.…”
mentioning
confidence: 99%
“…Increased levels of cytokines are also known to be linked to the pathophysiology of PSD [43]. Cerebral ischaemia leads to the production of increased proinflammatory IL-1β and TNF-α, which could further result in decreased 5-HT production, additionally promoting depression [44,45]. e cytokines could modulate 5-HT metabolism and HPA axis functionality, further modulating the pathophysiology of depression [46].…”
Section: Discussionmentioning
confidence: 99%