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Objective: To investigate the effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu (II) and Fe (II) ions. Methods: The antiproliferative effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu (II) and Fe (II) ions were examined by MTT assay. Additionally, colony-forming, reactive oxidative species (ROS) generation, apoptosis induction, autophagy, mitochondrial membrane potential, and mitochondrial mass were investigated. Results: At 24 and 72 h, no significant differences were observed in the viability of HepG2 cells between the control and syringic acid + Fe (II) groups. However, exposure of HepG2 cells to syringic acid + Cu (II) for 72 h reduced the cell viability significantly. Furthermore, ROS formation, induction of apoptosis, and autophagic vacuoles were significantly increased in HepG2 cells without marked changes in mitochondrial membrane potential and mitochondrial mass. Moreover, syringic acid + Cu (II) reduced the plating efficiency and surviving fraction significantly. Conclusions: The combination of syringic acid with Cu (II) was toxic to cancer cells and showed pro-oxidant activity. In addition, this combination induced autophagy in cancer cells with less cytotoxic effects on normal cells, which is a potential candidate for the development of novel therapeutics towards cancer.
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Objective: To investigate the effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu (II) and Fe (II) ions. Methods: The antiproliferative effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu (II) and Fe (II) ions were examined by MTT assay. Additionally, colony-forming, reactive oxidative species (ROS) generation, apoptosis induction, autophagy, mitochondrial membrane potential, and mitochondrial mass were investigated. Results: At 24 and 72 h, no significant differences were observed in the viability of HepG2 cells between the control and syringic acid + Fe (II) groups. However, exposure of HepG2 cells to syringic acid + Cu (II) for 72 h reduced the cell viability significantly. Furthermore, ROS formation, induction of apoptosis, and autophagic vacuoles were significantly increased in HepG2 cells without marked changes in mitochondrial membrane potential and mitochondrial mass. Moreover, syringic acid + Cu (II) reduced the plating efficiency and surviving fraction significantly. Conclusions: The combination of syringic acid with Cu (II) was toxic to cancer cells and showed pro-oxidant activity. In addition, this combination induced autophagy in cancer cells with less cytotoxic effects on normal cells, which is a potential candidate for the development of novel therapeutics towards cancer.
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Objective: To determine the effects of syringic acid on hepatic damage in diabetic rats. Methods: Diabetes was induced by streptozotocin. Diabetic rats were given syringic acid at doses of 25, 50 and 100 mg/kg by oral gavage for 6 weeks. Syringic acid effects on the liver were evaluated by examination of plasma biochemical parameters, and pathological study. In addition, biomarkers of lipid peroxidation and antioxidant status of liver tissues were assessed. Real time-PCR was performed to investigate the mRNA expression levels of mitochondrial biogenesis indices in different groups. Results: Syringic acid significantly attenuated the increase in most of plasma biochemical parameters in diabetic rats. Moreover, syringic acid treatment increased the catalase activity while it reduced the superoxide dismutase activity and hepatic malondialdehyde level in diabetic rats. There was no difference between the glutathione content of the treated and untreated groups. These findings were supported by alleviation of histopathological damages in the syringic acid-treated groups compared to the untreated diabetic group. Syringic acid also significantly up-regulated the hepatic mRNA expression of PGC-1a, NRF-1, and NRF-2 and increased the mtDNA/nDNA ratio in diabetic rats. Conclusions: Syringic acid can be considered as a suitable candidate against hepatic complications since it can reduce oxidative damages in diabetic cases. Furthermore, it has the potential of targeting hepatic mitochondria in diabetes.
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DNA damage is one of the most important consequences of oxidative stress in the cells. If DNA repair is unable to modify these inducible DNA damages, genomic instability may lead to mutation, cancer, aging and many other diseases. Single cell gel electrophoresis or comet assay is a common and versatile method to quantify these types of DNA damages. DNA damages induced by hydrogen peroxide (H
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Myrtus communis L. is a plant traditionally used as an antiseptic and disinfectant drug. In this research, the antioxidant activity of Myrtus communis was assayed by evaluating radical scavenging activity, reducing power, FRAP method and determination of phenolic compounds. The methanolic extract of leaves of Myrtus communis was fractionated by using petroleum ether, chloroform, ethyl acetate and buthanol. In reducing power, different concentrations of samples were mixed with phosphate buffer, ferrocyanate, TCA and ferric chloride. Different concentrations of samples were mixed with DPPH and after 30 min the absorbances were measured. For determination of phenolic content, 500 µl of sample was mixed with Folin-Ciocalteu and sodium carbonate. For determination of flavonoids, 500 µl of sample was mixed with 2 ml of distilled water, NaNO2 and NaOH. In reducing power method, chloroform fraction showed the highest reducing capacity. In the DPPH radical scavenging method, the highest antioxidant capacity was found in buthanol fraction [IC50=84.42 +/- 1.8 µg/ml]. In FRAP method, the highest antioxidant capacity was found in crude extract [5.4 +/- 0.3 mg/ml] and buthanol fractions [5.51 +/- 0.4 mg/ml], respectively. The highest amount of phenolic compounds was detected in ethyl acetate fraction of Myrtus communis [17.5 +/- 0.001 µg/g]. The highest amount of flavonoids was found in crude extract of Myrtus communis [171.9 +/- 7.3 µg/ml]. Overall, we can suggest that the leaves of Myrtus communis can be used as antioxidant and as a food additives to avoid oxidative degradation of foods