In vitro biological effects of Crataegus microphylla C. Koch

Cratageus species are rich in phenols and flavonoids, which are active compounds that possess beneficial effects. This study aimed to identify the antioxidant, antimicrobial, DNA damage protection activities, and the capacities of acetylcholinesterase (AChE), thioredoxin reductase (ThxR), and alpha-glucosidase inhibition of the methanol extract of Cratageus microphylla. The plant extract inhibited the formation of free radicals in various assay systems, such as 2,-2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), 2,2'-diphenyl-1-picrylhydrazyl (DPPH), lipid peroxidation (anti-LPO) and ferric reducing antioxidant power (FRAP) assays. According to the findings, the extract inhibited the lipid peroxidation and neutralized stable DPPH, and ABTS cation radicals with EC50 values of 0.766 +/- 0.026 mg/mL, 0.207 +/- 0.009 mg/mLand 0.756 +/- 0.048 mg/mL, respectively. The extract also acted as a reductant as indicated by the FRAP value (2.841 +/- 0.096 mM Fe2+), thus exhibiting its potential as an antioxidant. Moderate AChE (4.94 +/- 0.29 mg/mL) and a-glucosidase (14.41 +/- 0.29 mg/mL) and significant ThxR (EC50= 0.61 +/- 0.06 mg/mL) inhibition activities were observed. DNA damage formation in in vitro assays was 51 % at 0.78 mu g/mL concentrations. Therefore, C. microphylla can be considered as a good source of antioxidant, antimicrobial, antidiabetic, anticholinesterase, and anticancer agents

<i>In vitro</i> biological effects of <i>Crataegus microphylla</i> C. Koch

189-196Cratageus species are rich in phenols and flavonoids, which are active compounds that possess beneficial effects. This study aimed to identify the antioxidant, antimicrobial, DNA damage protection activities, and the capacities of acetylcholinesterase (AChE), thioredoxin reductase (ThxR), and α-glucosidase inhibition of the methanol extract of Cratageus microphylla. The plant extract inhibited the formation of free radicals in various assay systems, such as 2,-2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), 2,2'-diphenyl-1-picrylhydrazyl (DPPH), lipid peroxidation (anti-LPO) and ferric reducing antioxidant power (FRAP) assays. According to the findings, the extract inhibited the lipid peroxidation and neutralized stable DPPH, and ABTS cation radicals with EC50 values of 0.766 ± 0.026 mg/mL, 0.207 ± 0.009 mg/mLand 0.756 ± 0.048 mg/mL, respectively. The extract also acted as a reductant as indicated by the FRAP value (2.841 ± 0.096 mM Fe2+), thus exhibiting its potential as an antioxidant. Moderate AChE (4.94 ± 0.29 mg/mL) and α-glucosidase (14.41 ± 0.29 mg/mL) and significant ThxR (EC50= 0.61 ± 0.06 mg/mL) inhibition activities were observed. DNA damage formation in in vitro assays was 51 % at 0.78 µg/mL concentrations. Therefore, C. microphylla can be considered as a good source of antioxidant, antimicrobial, antidiabetic, anticholinesterase, and anticancer agents

Paraoxonase 2 overexpression inhibits tumor development in a mouse model of ovarian cancer

Abstract Ovarian cancer (OC) is most lethal malignancy among all gynecological cancer. Large bodies of evidences suggest that mitochondrial-derived ROS play a critical role in the development and progression of OC. Paraoxonase 2 (PON2) is a membrane-associated lactonase with anti-oxidant properties. PON2 deficiency aggravates mitochondrial ROS formation, systemic inflammation, and atherosclerosis. The role of PON2 in cancer development remains unknown. In this report, in human, we identified that PON2 expression is higher in early stages (but not in late stages) of OC when compared to normal tissue. Using a mouse xenograft model of OC, we demonstrate that overexpression of PON2 prevents tumor formation. Mechanistically, PON2 decreases OC cell proliferation by inhibiting insulin like growth factor-1 (IGF-1) expression and signaling. Intriguingly, PON2 reduces c-Jun-mediated transcriptional activation of IGF-1 gene by decreasing mitochondrial superoxide generation. In addition, PON2 impairs insulin like growth factor-1 receptor (IGF-1R) signaling in OC cells by altering cholesterol homeostasis, which resulted in reduced caveolin-1/IGF-1R interaction and IGF-1R phosphorylation. Taken together, we report for the first time that PON2 acts as a tumor suppressor in the early stage of OC by reducing IGF-1 production and its signaling, indicating PON2 activation might be a fruitful strategy to inhibit early stage ovarian tumor