Either elevated expression of or partial loss of SIRT1 inhibited cell proliferation and induced cell apoptosis. Accumulation of BAX and cleaved CASPASE-8/9/3, inhibition of PGC-1α/NRF2 pathway, increase oxidative stress and reduction of BCL-2 as well as uncleaved PARP were found in the presence of or the absence of . Overexpression of could reduce anti-proliferative and pro-apoptotic effects of . Overall, this study concluded that -dependent inhibition displays anti-proliferative and proapoptotic roles in PC cells via PGC-1α/NRF2 pathway, which highlights as a potential target for PC treatment.Overall, this study concluded that miR-373-dependent SIRT1 inhibition displays anti-proliferative and proapoptotic roles in PC cells via PGC-1α/NRF2 pathway, which highlights miR-373 as a potential target for PC treatment. Research suggests that fine particulate matter (PM2.5) contributes to the expansion and development of atherosclerosis. Infiltration and proliferation of vascular smooth muscle cells (VSMCs) from the blood vessel media into the intima, is an important step in the atherosclerosis pathophysiology. Afrocyclamin A, is an oleanane-type triterpene saponin, isolated from , which is commonly used in Chinese herbal medicine. In the study, we examined the effect of Afrocyclamin A on PM2.5-induced VSMCs proliferation and scrutinized possible mechanisms of action. In the experimental study, counting Kit-8 (CCK-8) assay was used for estimation of VSMCs viability. BrdU immunofluorescence was used for estimation of VSMCs proliferation. The levels of antioxidant parameters such as malonaldehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH); proinflammatory cytokines such as interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), nitric oxide (NO), endothelin-1 (ET-1), and vascular cell adhesion molecule-1 (VCAM-1), were estimated. The expression of proliferating cell nuclear antigen (PCNA) and phospho-p38 MAPK (p-p38 MAPK) was assessed. Compared to PM2.5-treated cells, in addition to reducing PM2.5-induced VSMCs proliferation, Afrocyclamin A reduced the expression of PCNA and p-p38 MAPK, down-regulated the level of TNF-α, IL-1β, IL-6, VCAM-1, MDA and ET-1, and up-regulated SOD, GSH and NO level. Furthermore, the anti-proliferative effect of Afrocyclamin A was considerably increased following co-incubation of Afrocyclamin A with SB203580 (p38 MAPK inhibitor) in comparison with Afrocyclamin A-treated cells. Based on the results, we can conclude that Afrocyclamin A might reduce PM2.5-induced VSMCs proliferation via reduction of p38 MAPK signaling pathway.Based on the results, we can conclude that Afrocyclamin A might reduce PM2.5-induced VSMCs proliferation via reduction of p38 MAPK signaling pathway. Quercetin (Que) is a plant-derived polyphenolic compound, that was shown to possess anti-inflammatory activity in myocardial ischemia/reperfusion (I/R) models ; however, detailed mechanisms of its anti-inflammatory effects remain unclear. This study aimed to examine the effects of quercetin postconditioning (QPC) on I/R-induced inflammatory response in a rat model and evaluate the role of the mitochondrial K-ATP (mitoK ) channels and NO system in this regard. In this experimental study, hearts of male Wistar rats (250 ± 20 g) perused by Langendorff apparatus, were subjected to 30 minutes of global ischemia followed by 55 minutes reperfusion, and Que was added to the perfusion solution immediately at the onset of reperfusion. Creatine kinase (CK) levels in the coronary effluent were measured by spectrophotometry. Interleukin-1 (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α) levels were analyzed by an enzyme-linked immunosorbent assay (ELISA) rat specific kit to assess the inflammatory condition oKATP channels and NO system might be involved in this anti-inflammatory effect. The aim is to examine the effect of metformin in human microvascular endothelial cells exposed to high glucose (HG) concentration and compare them with the effects of other 5' adenosine monophosphate-activated protein kinase (AMPK) modulators under the same condition. In this experimental study, human microvascular endothelial cells (HMECs) were treated with 15 mM metformin, 1 mM 5-aminoimidazol-4-carboxamideribonucleotide (AICAR) and 10 mM compound C in the presence of 20 mM glucose (hyperglycemic condition). Migration, invasion and proliferation were evaluated as well as the capillary-like structures formation. Moreover, the expression of angiogenic genes was assessed. Metformin significantly inhibited vessel formation and migration, although it did not change HMECs proliferation and invasion. In addition, metformin significantly reduced collagen formation as evidenced by histological staining. Concomitantly, expression of several genes implicated in angiogenesis and fibrosis, namely and , was slightly upregulated. Epigenetics inhibitor Immunostaining for proteins involved in ALK5 receptor signaling, the alternative TGFß signaling pathway, revealed significant differences in SMAD2/3 expression. Our data showed that metformin prevents vessel assembly in HMECs, probably through an AMPKindependent mechanism. Understanding the molecular mechanisms by which this pharmacological agent affects endothelial dysfunction is of paramount importance and paves the way to its particular use in preventing development of diabetic retinopathy and nephropathy, two processes where angiogenesis is exacerbated.Our data showed that metformin prevents vessel assembly in HMECs, probably through an AMPKindependent mechanism. Understanding the molecular mechanisms by which this pharmacological agent affects endothelial dysfunction is of paramount importance and paves the way to its particular use in preventing development of diabetic retinopathy and nephropathy, two processes where angiogenesis is exacerbated. Alpha-lipoic acid (ALA) as a strong antioxidant has a protective effect. This study was designed to assess whether supplementation of maturation medium with ALA during maturation (IVM) can attenuate the toxic effect of ethanol. In this experimental study, to assess the antioxidant capacity of ALA challenged by 1% ethanol during maturation, immature ovine oocytes were exposed to 1% alcohol in the presence or absence of 25 μM ALA during oocyte maturation. The cumulus expansion index, intracellular reactive oxygen species (ROS), and thiol content levels were assessed in matured oocytes of various treatment groups. Consequently, the blastocyst formation rate of matured oocytes in various treatment groups were assessed. In addition, total cell number (TCN), cell allocation, DNA fragmentation, and relative gene expression of interested genes were assessed in resultant blastocysts. The results revealed that alcohol significantly reduced cumulus cells (CCs) expansion index and blastocyst yield and rate of apoptosis in resultant embryos.