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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی:
- چکیده:
- چکیده انگلیسی: The liver is continuously exposed to a variety of xenobiotics. Several xenobiotics are identified which act as hepatotoxicants. Hence, finding protective agents for ameliorating xenobiotics-included liver injury has a great value. Eisenia foetida, a kind of “earthworm,” is a source of a wide range of bioactive components. Several investigations have been evaluated the E. foetida extract (EFX) for biomedical and nutritional applications. The current study was designed to evaluate the potential hepatoprotective properties of EFX in two experimental models of hepatic damage. Acetaminophen (APAP; 1 g/kg, i.p) was administered as the animal model of acute liver injury in mice. Bile duct ligated (BDL) rats were used as the animal model of chronic hepatic damage. Severe elevation in tissue biomarkers of oxidative stress including lipid peroxidation and hepatic glutathione depletion was evident in both APAP-treated and BDL animals. Moreover, serum biomarkers of liver injury were drastically increased in both acute and chronic animal models of hepatotoxicity. Significant liver tissue histopathological alterations including tissue necrosis, vascular congestion, and inflammatory cells infiltration were detected in APAP-treated and BDL animals. On the other hand, it was found that EFX supplementation (100, 200, 500, and 700 mg/kg, i.p) mitigated oxidative stress markers, decreased serum biomarkers of liver injury, and alleviated liver tissue histopathological changes. The hepatoprotection provided by EFX supplementation in the current study might be mediated through its potential antioxidative mechanisms.
- انتشار مقاله: 10-06-1397
- نویسندگان: Akram Jamshidzadeh,Fatemeh Dabagh,Omid Farshad,Mohammad Mehdi Ommat,Azadeh Mahdavinia,Negar Azarpira,Maryam Shahbazi,Asma Najibi,Reza Heidari
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: oxidative stress,Hepatoprotective,hepatotoxicity,Glutathione,Sodium Valproate
- چکیده:
- چکیده انگلیسی: Valproic acid (VPA) is a widely administered drug against epilepsy and several other neurological disorders. On the other hand, liver injury is a deleterious side effect associated with VPA. Oxidative stress seems to play a critical role in VPA-induced hepatotoxicity. The current investigation was designed to evaluate if N-acetylcysteine (NAC) and dithiothreitol (DTT) as thiol reducing agents have any protective effects against VPA-induced liver injury. Isolated rat hepatocytes (in vitro) were exposed to increasing concentrations of VPA (25, 50, 100, 150, and 250 µM) and markers of cytotoxicity were evaluated. Furthermore, animals received VPA (250 and 500 mg/kg, i.p for 15 consecutive days) (in vivo) and markers of liver injury were monitored. It was found that 250 µM of VPA caused marked cytotoxicity toward isolated hepatocytes as judged by trypan blue exclusion test. Moreover, markers of oxidative stress including glutathione depletion and lipid peroxidation were detected in VPA-treated hepatocytes. On the other hand, VPA caused a significant increase in plasma markers of hepatotoxicity in drug-treated group. Liver histopathological changes and markers of oxidative stress were also detected in VPA-treated animals. It was found that administration of NAC (1 mM), and DTT (1 mM) significantly alleviated VPA-induced cytotoxicity (In vitro). NAC (250 and 500 mg/kg) and DTT (15 and 30 mg/kg) also significantly mitigated VPA hepatotoxicity (In vivo). The data obtained from the current investigation indicate potential therapeutic properties of thiol reductants against VPA-induced liver injury.
- انتشار مقاله: 11-02-1396
- نویسندگان: Nahid Najafi,Akram Jamshidzadeh,Hamideh Fallahzadeh,Mahmoud Omidi,Narges Abdoli,Asma Najibi,Negar Azarpira,Reza Heidari,Hossein Niknahad
- 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: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Medicinal plants,Hepatoprotective,hepatotoxicity,Liver injury,Gundelia tournefortii
- چکیده:
- چکیده انگلیسی: Xenobiotics-induced liver injury is a major challenge for clinicians and pharmaceutical industry. Hence, finding new therapeutic molecules against this complication has clinical value. The current investigation aimed to evaluate the potential protective effects of different fractions obtained from Gundelia tournefortii (GT) hydroalcoholic extract in a rat model of acute hepatic injury. Male Sprague-Dawley rats (200‑250 g) were treated with carbon tetrachloride (CCl4) (1.5 ml/kg, i.p), then ethanol, water, chloroform, ethyl acetate, and n-Butanol fractions of GT extract were administered. Biochemical and histopathological markers of hepatic injury were assessed and glutathione (GSH) and lipid peroxidation were monitored in liver samples. CCl4 administration caused hepatotoxicity as revealed by an increase in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activity, as well as pathological changes of the liver. Furthermore, a significant reduction in hepatic glutathione content and an elevation in lipid peroxidation were observed in CCl4‑treated rats. It was found that the n‑butanol (200 mg/kg) and the ethyl acetate (300 mg/kg) fractions of GT extract protected liver against CCL4‑induced damage as judged by lower AST, ALT, LDH and lipid peroxidation, prevention of tissue glutathione depletion, and alleviation of histopathological damages of liver in extract‑treated animals. As n‑butanol and the ethyl acetate fractions of GT effectively alleviated the liver injury induced by CCl4 and provide antioxidant properties, we might be able to propose that the hepatoprotective chemicals of Gundelia extract are present in these fractions.
- انتشار مقاله: 12-10-1394
- نویسندگان: Hossein Niknahad,Reza Heidari,Tannaz Mokhtebaz,Sasan Mansouri,Shadab Dehshahri,Narges Abdoli,Asma Najibi
- مشاهده