Proposed mechanisms include reduced α1-receptor density and reduced α1-adrenergic signal transduction [34], activation of vascular KATP channels [33], impaired SR Ca2+ release [15,35], relative corticosteroid and vasopressin deficiency [36,37] and activation of inducible nitric oxide synthase [38] and vasodilating inflammatory mediators [39-42] [39-42]
Proposed pathophysiologic mechanisms include reduced transglomerular pressure, elevated renal interstitial pressure, myogenic and neural reflexes, activation of sympathetic nervous and renin-angiotensin-aldosterone systems, non-osmotic release of arginine vasopressin, local production of endothelin, and enhanced proinflammatory pathways.
Possible important pathophysiological mechanisms include reduced regional/global cerebral blood flow (CBF) indicative of chronic ischemia [ 4- 8], impaired intracranial compliance (ICC) [ 9- 12], and impaired cerebral pulsation absorber capacity causing cerebral capillary damage [ 13, 14].
MDR can result from several distinct mechanisms, including reducing drug accumulation in tumor cells [1].
It may be activated through several cellular mechanisms, including reducing BubR1 protein levels [ 11, 26, 27], increasing ER-α transcription [ 28, 29], activating RHO GTPase [ 30], MAPK and ElK1 [ 31], inducing MMP expression [ 32], and constitutive activation of ERK1/2 [ 19].
Moreover, multiple mechanisms, including reducing the expression ratio of TGF-β1/BMP-7 and inhibiting the excessive activation of Hh signaling pathway, were involved in modulating the balance between EMT and MET by DWYG treatment, which further demonstrate the advantage of traditional Chinese medicine compound with multi-component and multi-target in the therapy for liver fibrosis.
This is in line with the knowledge that phenolics confer anti-diabetic effects via various mechanisms, including reducing oxidative stress and lipid peroxidation, defending pancreatic cells from oxidative damage, protecting lymphocytes from DNA damage, as well as preserving vascular functions in diabetic complications.
CS induces lung inflammation through different types of mechanisms, including reduced fibroblast proliferation and migration, and genetic mutations in the lung [ 3– 6].
This latter phenomenon is known as multidrug resistance (MDR) and can be conveyed by several mechanisms including reduced drug uptake, activation of DNA repair and defective apoptotic pathways.
134, 135 Therefore, amongst other effects, amylase inhibition could modulate GI function and gut peptide release, strengthening satiety and decreasing food intake by mechanisms including reduced gastric emptying.
