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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Anti-inflammatory,Citrus aurantium,linoleic acid,seed oil,bitter orange,phytosterols
- چکیده:
- چکیده انگلیسی: The present investigation was carried out to evaluate the pharmacognostic properties of Citrus aurantium seeds as well as its anti-inflammatory activities. The n-hexane fraction of seed oil extracted via a Soxhlet extractor and subjected to pharmacognostic assays, HPTLC and GC-MS analysis for determination of fatty acids and sterols. The possible anti-inflammatory and antinociceptive activities in rats were evaluated using formalin-induced paw licking, oedema and myeloperoxidase activity assessment. Total ash, acid insoluble and water soluble ash values were determined as 35.83 ± 4.92, 6.67 ± 2.89 and 28.33 ± 5.77 mg/g, respectively. HPTLC assessment revealed the presence of different fatty acids and steroidal triterpenes. The principal fatty acids of the seed oil were linoleic acid (C18:2, 50.10 ± 2.58 %) and Oleic acid (C18:1, 30.14 ± 0.39). Esterified (2.40 mg/g) and free β-sitosterol (32.90 mg/g), free campesterol (3.9 mg/g) and free stigmasterol (10.165 mg/g) were detected in the oil. Seed oil exhibited anti-inflammatory properties in the first and the second phases of formalin test. Also, it had anti-edematogenic effects but exerted no effects on myeloperoxidase activity.
- انتشار مقاله: 10-05-1398
- نویسندگان: Azadeh Hamedi,Mohammad M. Zarshenas,Akram Jamshidzadeh,Saeed Ahmadi,Reza Heidari,Ardalan Pasdaran
- مشاهده
- 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:
- چکیده:
- چکیده انگلیسی: Heavy metals are environmental pollutants which pose toxicity toward biological systems. Most organs are susceptible to heavy metals-induced toxicity. Hence, finding protective agents against heavy metals-induced toxicity is valuable. The post-nuclear supernatant (PNS) has been accepted as an in vitro model for assessing xenobiotic-induced toxicity toward biological systems. Monitoring the toxic effects of a large number of xenobiotics in a short time is one of the superiorities of PNS system. The goal of the present study was to validate the PNS as an in vitro model for investigating the effect of heavy metals (Cd, Co, Cu, Fe, As, Hg, Cr, and Pb)-induced toxicity and evaluating the potential protective effects of glycine and betaine. Markers of oxidative stress including ROS formation, lipid peroxidation and glutathione content in addition of succinate dehydrogenase activity (MTT test) were monitored in the presence of heavy metals alone or in combination with glycine (1 mM) and betaine (100 µM). Our results suggest that PNS preparations can be used as an appropriate model for future investigation of xenobiotics-induced toxicity and estimation of the protective properties of different agents. Indeed, further evaluations in other experimental models could reveal the protective properties of betaine and glycine against heavy metals-induced organ injury.
- انتشار مقاله: 12-03-1397
- نویسندگان: Reza Heidari,Hamidreza Mohammadi,Asrin Ahmadi,Vahid Ghanbarinejad,Faraz Kasra,Amir Khosravi
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی:
- چکیده:
- چکیده انگلیسی: Carnosine is an abundantly found dipeptide present in different tissues. Several pharmacological properties have been attributed to carnosine. On the other hand, the precise mechanism of cytoprotection provided by carnosine remains obscure. The current study aimed to evaluate the direct effect of different concentrations of carnosine on cellular mitochondria as an essential target involved in the cytoprotection/cytotoxicity. Liver mitochondria were isolated and exposed to carnosine (0.01-20 mM). Mitochondrial depolarization, dehydrogenases activity, mitochondrial swelling and permeability, and ATP content were assessed. On the other hand, the effect of carnosine supplementation on calcium (Ca2+) overload-induced mitochondrial injury was evaluated. It was found that concentrations between 0.01-20 mM of this peptide preserved mitochondrial indices of functionality in a Ca2+ overloaded environment. These data represent regulation of mitochondrial function as a primary mechanism for the protective properties of carnosine.
- انتشار مقاله: 30-11-1396
- نویسندگان: Reza Heidari,Vahid Ghanbarinejad,Mohammad Mehdi Ommati,Akram Jamshidzadeh,Hossein Niknahad
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی:
- چکیده:
- چکیده انگلیسی: The cholestatic liver disease ensues with a hepatic accumulation of cytotoxic molecules. Several hydrophobic bile acids are known as cytotoxic agents accumulated in the liver during cholestasis. Chenodeoxycholic acid (CDCA) is a toxic hydrophobic bile acid. Oxidative stress and mitochondrial dysfunction are well-known mechanisms of bile acids cytotoxicity. In the current study, CDCA effect on isolated liver mitochondria was monitored by analyzing the changes in mitochondrial dehydrogenases activity, mitochondrial permeabilization, and mitochondrial membrane potential. On the other hand, taurine (1 mM) and carnosine (1 mM) were added as potential protective agents against CDCA-induced mitochondrial dysfunction. Increasing concentrations of CDCA (100 µM - 1000 µM) impaired mitochondrial membrane potential, decreased mitochondrial dehydrogenases activity and enhanced mitochondrial permeabilization and swelling. It was found that taurine and carnosine supplementation preserved mitochondrial function in the presence of CDCA. The results mention that toxicologically relevant concentrations of CDCA impaired mitochondrial function. On the other hand, taurine and carnosine might be applicable as protective agents against bile acids-induced mitochondrial impairment and toxicity.
- انتشار مقاله: 12-03-1397
- نویسندگان: Reza Heidari,Narges Abdoli,Mohammad Mehdi Ommati,Akram Jamshidzadeh,Hossein Niknahad
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی:
- چکیده:
- چکیده انگلیسی: The xenobiotics-induced liver injury is a major clinical complication. Hence, finding hepatoprotective agents could have clinical value. Herbal medicines are a major source of biologically active chemicals which could be applied as hepatoprotective agents. The current study was designed to assess the hepatoprotective properties of Avicennia Marina (AM) extract and its different fractions. In vivo, the hepatoprotective effect of AM total extract against CCl4-induced acute liver injury was evaluated in rats, and a series of histopathological, biochemical, and oxidative stress parameters were monitored. In vitro, the protective effect of AM extract fractions (Petroleum ether, Chloroform, Ethyl acetate, and Ethanol) was evaluated on human liver hepatoma cells (HepG2). Severe elevation in serum level of liver injury biomarkers, along with liver tissue histopathological changes, lipid peroxidation, and liver tissue glutathione depletion were detected in CCl4-treated rats. On the other hand, CCl4-induced toxicity was evident in vitro by significant cell death. It was found that AM extract provided significant protection against CCL4 toxicity in vivo by decreasing serum biomarkers of liver injury and tissue markers of oxidative stress. In vitro, the protective effect of AM extract fractions (Chloroform, Ethyl acetate, and Ethanol) was evident as these fractions significantly decreased CCl4 cytotoxicity. As AM extract exhibited significant suppression of oxidative stress markers, its antioxidant effect could play a significant role in its hepatoprotective properties.
- انتشار مقاله: 29-08-1396
- نویسندگان: Omid Farshad,Reza Heidari,Hamidreza Mohammadi,Amin Reza Akbarizadeh,Mohammad M. Zarshenas
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی:
- چکیده:
- چکیده انگلیسی: Hepatic encephalopathy (HE) is a serious clinical complication, which could lead to coma and death if not appropriately managed. There is agreement on the predominant role of ammonia in the etiology of HE. Brain is one of the most critical organs affected by ammonia. The critical role of oxidative stress and its consequences in the pathogenesis of ammonia-induced brain injury have been revealed before. On the other hand, there is no promising therapeutic option against ammonia neurotoxicity. Taurine is one of the most abundant amino acids in the human body. Several pharmacological roles including brain protecting properties have been attributed to this amino acid. The current study was designed to evaluate the role of taurine supplementation on HE-induced oxidative stress in the brain tissue. Animals received thioacetamide (400 mg/kg, i.p, for three consecutive days at 24-hr intervals) as a model of acute liver failure and hyperammonemia. Several serum biochemical parameters, in addition to plasma and brain ammonia level, were monitored. Moreover, markers of oxidative stress in the brain of hyperammonemic animals were assessed. It was found that plasma and brain ammonia was increased, and serum markers of liver injury were significantly elevated in the thioacetamide-treated group. On the other hand, an increase in markers of oxidative stress, including reactive oxygen species formation, lipid peroxidation, glutathione depletion, and decreased tissue antioxidant capacity, was detected in the brain tissue of thioacetamide-treated animals. It was found that taurine treatment (250, 500, and 1000 mg/kg, i.p) alleviated brain tissue markers of oxidative stress and decreased serum biomarkers of liver injury. Furthermore, lower plasma and brain ammonia were detected in taurine-treated animals. These data suggest taurine as a potential protective agent with therapeutic capability against HE-associated central nervous system complications.
- انتشار مقاله: 11-06-1396
- نویسندگان: Akram Jamshidzadeh,Narges Abdoli,Hossein Niknahad,Negar Azarpira,Elnaz Mardani,Somayeh Mousavi,Mojgan Abasvali,Reza Heidari
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی:
- چکیده:
- چکیده انگلیسی: Fulminant hepatic failure is a deleterious clinical complication, which leads to hyperammonemia. Ammonia is a noxious neurotoxic agent, which affects brain tissue through different mechanisms. On the other hand, it is well-known that oxidative stress and its consequences play a major role in the pathogenesis of ammonia-induced brain injury. Carnosine is a dipeptide abundantly found in the human central nervous system (CNS). This peptide is widely investigated for its neuroprotective properties. The current study aimed to evaluate the effect of carnosine supplementation on oxidative stress markers in the brain tissue of a rat model of fulminant hepatic failure and hyperammonemia. Animals received thioacetamide (400 mg/kg, i.p, for three consecutive days at 24-hr intervals) as a model of acute liver failure and hyperammonemia. Several serum biochemical parameters, in addition to plasma and brain ammonia level, were monitored. On the other hand, brain tissue markers of oxidative stress including reactive oxygen species (ROS) formation, lipid peroxidation, tissue glutathione content, and total antioxidant capacity were measured. It was found that plasma and brain ammonia was increased, and serum markers of liver injury were significantly elevated in the thioacetamide-treated group. On the other hand, an increase in markers of oxidative stress, including ROS formation, lipid peroxidation, glutathione depletion, and decreased tissue antioxidant capacity, was evident in the brain of thioacetamide-treated animals. It was found that carnosine supplementation (250, 500, and 1000 mg/kg) decreased serum markers of liver injury, mitigated brain, and plasma ammonia level, and alleviated brain tissue markers of oxidative stress. These data suggest carnosine as a potential neuroprotective agent with therapeutic capability against ammonia-induced CNS injury.
- انتشار مقاله: 11-06-1396
- نویسندگان: Akram Jamshidzadeh,Narges Abdoli,Hossein Niknahad,Negar Azarpira,Somayeh Mousavi,Elnaz Mardani,Mojgan Abasvali,Reza Heidari
- مشاهده
- جایگاه : پژوهشی
- مجله: Trends in Pharmaceutical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: chemotherapy,hepatotoxicity,Antineoplastic agents,Glutathione,Drug-Induced Liver Injury (DILI)
- چکیده:
- چکیده انگلیسی: Mitoxantrone is anthracycline antibiotic highly effective against various human cancers. Hepatotoxicity is associated with mitoxantrone administration. On the other hand, there is no effective therapeutic option against chemotherapy-induced liver injury. The current investigation was designed to evaluate the effect of thiol reductants on mitoxantrone-induced liver injury in two experimental models. As an ex vivo model, isolated rat liver was exposed to increasing concentrations of mitoxantrone (100, 250, 750, and 1000 µM) alone or in combination with thiol-reductants (Dithiothreitol; DTT, and N-acetyl cysteine; NAC). In addition, rats (in vivo) received mitoxantrone (2.5 mg/kg, i.p, at days 1, 10, and 20), NAC (100 and 300 mg/kg/day, i.p, for 20 consecutive days) and DTT (15 and 30 mg/kg/day, i.p, for 20 consecutive days), then liver and serum pathological changes were monitored. Mitoxantrone-induced liver injury was evident in both ex vivo and in vivo experiments as assessed by pathological changes in biomarkers of liver injury, along with tissue histopathological changes. Furthermore, an increase in liver tissue markers of oxidative stress was detected in the mitoxantrone-treated group. It was found that thiol reductants significantly mitigated mitoxantrone hepatotoxicity. The data indicate that thiol reductants might serve as hepatoprotective agents against chemotherapy-induced liver injury.
- انتشار مقاله: 11-02-1396
- نویسندگان: Hossein Niknahad,Helia Hosseini,Fatemeh Gozashtegan,Farzaneh Ebrahimi,Negar Azarpira,Narges Abdoli,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