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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Neurodegeneration,oxidative stress,ATP,Neurotoxicity,Mitochondrial impairment
- چکیده:
- چکیده انگلیسی: Multiple sclerosis (MS) is a neurodegenerative disease. Although multiple factors are involved in the pathogenesis of MS, there are several lines of evidence that oxidative stress and mitochondrial dysfunction are involved in neuronal demyelination and deterioration of MS symptoms. Hence, compounds that could modulate mitochondrial function and decrease mitochondria-mediated ROS formation might be able to decrease MS symptoms. Methylene blue (MB) is a compound widely used in the treatment of central nervous system disease (e.g., Alzheimer's disease). It has been found that MB could robustly suppress mitochondria-mediated ROS formation at low concentrations. The current study was designed to evaluate the effect of MB on neuronal demyelination, mitochondrial function, and ROS formation in an animal model of MS. C57BL/6 male mice received cuprizone (0.1% w: w in chow diet for 42 consecutive days). MB (0.5 and 1 mg/kg, oral) was simultaneously administered. Significant demyelination was detected in CPZ-treated animals, which confirm the induction of MS in the mice model. Decreased animals’ locomotor activity, including significant suppression of open field movement, stride length, and decreased time on the rotarod, was evident in CPZ-treated mice. Mitochondrial indices, including significantly elevated lipid peroxidation, mitochondrial depolarization, significant mitochondrial permeabilization, and decreased ATP levels, were also detected in the CPZ group. It was found that MB administration significantly improved animals’ locomotor activity and mitochondrial indices in the current animal model of MS. The effects of MB on mitochondria and mitochondria-mediated ROS formation might play a fundamental role in the protective effects of this compound.
- انتشار مقاله: 10-12-1398
- نویسندگان: Mohammad Mehdi Ommati,Negar Azarpira,Forouzan Khodaei,Hossein Niknahad,Vahideh Gozashtegan,Reza Heidari
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: cancer,chemotherapy,amino acid,hepatotoxicity,Hepatoprotection,Drug-Induced Liver Injury (DILI)
- چکیده:
- چکیده انگلیسی: Taurine (2-aminoethane sulfonic acid) is a non-protein amino acid found in high concentration in different tissues. Glycine (Amino acetic acid) is the simplest amino acid incorporated in the structure of proteins. Several investigations indicate the hepatoprotective properties of these amino acids. On the other hand, antineoplastic agents-induced serum transaminase elevation and liver injury is a clinical complication. The current investigation was designed to screen the possible hepatoprotective properties of taurine and glycine against antineoplastic drugs-induced hepatic injury in an ex vivo model of isolated perfused rat liver. Rat liver was perfused with different concentration (10 µM, 100 µM and 1000 µM) of antineoplastic drugs (Mitoxantrone, Cyclophosphamide, Cisplatin, 5‑Fluorouracil, Doxorubicin and Dacarbazine) via portal vein. Taurine and glycine were administered to drug-treated livers and liver perfusate samples were collected for biochemical measurements (ALT, LDH, AST, and K+). Markers of oxidative stress (reactive oxygen species formation, lipid peroxidation, total antioxidant capacity and glutathione) were also assessed in liver tissue. Antineoplastic drugs caused significant pathological changes in perfusate biochemistry. Furthermore, markers of oxidative stress were significantly elevated in drug‑treated livers. It was found that taurine (5 and 10 mM) and glycine (5 and 10 mM) administration significantly mitigated the biomarkers of liver injury and attenuated drug‑induced oxidative stress. Our data indicate that taurine and glycine supplementation might help as potential therapeutic options to encounter anticancer drugs-induced liver injury.
- انتشار مقاله: 12-10-1394
- نویسندگان: Reza Heidari,Akram Jamshidzadeh,Hossein Niknahad,Farshad Safari,Hamdollah Azizi,Narges Abdoli,Mohammad Mehdi Ommati,Forouzan Khodaei,Arastoo Saeedi,Asma Najibi
- مشاهده
- جایگاه : پژوهشی
- مجله: Research Journal of Pharmacognosy
- نوع مقاله: Journal Article
- کلمات کلیدی: Mitochondria,Apoptosis,Sirt3,ROS,Capparis spinosa
- چکیده:
- چکیده انگلیسی: Background and objectives: Beside its nutritional role, caper (Capparis spinosa) has long been used as an analgesic, anti-inflammatory, anti-diabetic and anti-cancer remedy. In the present study, we tested whether this plant can make effective changes in Sirt3 and mitochondrial function in colorectal carcinoma cell line since mitochondrial dysfunction has long been implicated in both cancer and diabetes and benefit confers by caper in these diseases might be due to mitochondrial alterations. Methods: Total flavonoids and phenolics were assayed using colorimetric tests. Cytotoxicity of a phenolic-flavonoid rich extract of caper collected from two different geographical regions (south and west) were mechanistically studied in HT-29 cell line. Activity of an essential mitochondrial enzyme, Sirt3 has also been evaluated along with other parameters. IC50 of extracts were determined by MTT cytotoxicity assay, cell death and mitochondrial membrane potential were evaluated via flow cytometric analysis. Also, at IC50 concentrations, Sirt3 activity was determined fluorimetrically. Results: The results showed that caper induced significant cytotoxicity in HT-29 cells followed by mitochondrial membrane potential collapse, ROS overproduction, Sirt3 activity alteration and cell death. Conclusions: The above-mentioned cytotoxic parameters were inversely proportional to the phenolic and flavonoid contents of the extract showing that other mechanisms beyond their antioxidant capacities may contribute to their anti-cancer effects. In other term, these results suggest that antioxidant capacity may not directly contribute to the anticancer property.
- انتشار مقاله: 05-06-1396
- نویسندگان: Forouzan Khodaei,Mohsen Rezaei*,Mahmoud Hashemitabar,Marzieh Jafari,Amir Siahpoosh,Mahmood Reza Moein
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Apoptosis,Teucrium Polium,Prosopis Farcta,Sirt3,ROS
- چکیده:
- چکیده انگلیسی:
Background: Teucrium Polium and Prosopis Farcta have been traditionally employed in cancer treatment. In this study we evaluated the effects of methanolic extracts of these two plants in HT-29 cells. Methods: IC50s of extracts were obtained via MTT assay and the levels of ROS production, cell death, collapse of mitochondrial membrane potential and Sirt3 enzyme activity were determined. Results: After 48 hours exposure, IC50s for Teucrium and Prosopis extracts were 3 and 2μg/ml, respectively. Extracts induced higher ROS production after 6 hours than after 12 hours. Mitochondrial membrane potential collapse and cell death rate were also increased; Teucrium caused greater cell death than Prosopis. Extracts from both plants increased Sirt3 activity in its normal form, but only Teucrium extract caused a significant increase in activity of Sirt3 enzyme isolated from cancer cells. Conclusion: Teucrium and Prosopis extracts exert anticancer activity via mitochondrial alterations, as exemplified by increased ROS levels, Sirt3 activity and cell death in HT-29 colorectal cancer cells.- انتشار مقاله: 03-05-1396
- نویسندگان: Forouzan Khodaei,Kiyanoosh Ahmadi,Hamze Kiyani,Mahmoud Hashemitabar,Mohsen Rezaei
- مشاهده