در هنگام جستجو کلمه در قسمت عنوان میتوانید کلمات مورد جستجو را با کاراکتر (-) جدا کنید.
کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Research Journal of Pharmacognosy
- نوع مقاله: Journal Article
- کلمات کلیدی: analgesics,Anti-inflammatory agents,Rosaceae,Geum
- چکیده:
- چکیده انگلیسی: Background and objectives:Traditionally, Geum species from Rosaceae family have been used for treating inflammatory disorders. Geum iranicum Khatamsaz is endemic to Iran. The aim of this study was to investigate the antinociceptive and anti-inflammatory activities of Geum iranicum methanol extract G. iranicum methanol extract using classical models. Methods: The methanol extract of G. iranicum roots was evaluated for antinociceptive activity by acetic acid-induced writhing, formalin and hot-plate tests in male Swiss albino mice. The anti-inflammatory effect was investigated by Carrageenan-induced paw edema method. Results: The extract significantly inhibited both the first and second phases of formalin-induced nociception in mice at the dose of 100 mg/kg compared to the control group. In acetic acid-induced writhing test and hot plate method, the extract significantly reduced pain behavior in all doses (25, 50 and 100 mg/kg). The antinociceptive activity of the extract was significantly reduced by naloxone (4 mg/kg). The anti-inflammatory activity of the extract was found to be dose dependent. The extract at the dose of 100 mg/kg exhibited significant reduction of paw edema in all surveyed times. Conclusion: The results showed that the methanol extract of G. iranicum roots possessed central analgesic activity via modulation of opioid receptors as well as anti-inflammatory activity. The observed effects could be attributed to the presence of constituents like triterpenoids, eugenol, sucrose and tannins in the extract.
- انتشار مقاله: 09-11-1397
- نویسندگان: Nematollah Ahangar,Fatemeh Mirzaee,Maryam Feizbakhsh,Sara Pirhayati,Somayeh Shahani*
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Acetaminophen,Hypothermia,Abinitio study,Benzodiazepine receptor,GABAA
- چکیده:
- چکیده انگلیسی: Objective(s):The mechanism of hypothermia action of acetaminophen (APAP) remains unclear even 125 years after its synthesis. Acetaminophen produces hypothermia. The mechanism of this reduction in core body temperature is not clear but evidence shows that it is not dependent on opioid and cannabinoid receptors. Because of strong documents about the roles of GABA and benzodiazepine receptors in hypothemic activity of some drugs such as diazepam, we determined if these receptors also contributes to the hypothermic effect of APAP. Materials and Methods: Diazepam (5 mg/kg, IP) was used for induction of hypothermia. Flumazenil (10 mg/kg, IP) or picrotoxin (2 mg/kg, IP) used for reversal of this effect. Rats injected with APAP (100, 200 or 300 mg/kg, IP). Baseline temperature measurements were taken with a digital thermometer via rectum. To evaluate the structural correlation between APAP and benzodiazepine receptor ligands, numerous models are selected and studied at HF/6-31G* level of theory. Relative energies, enthalpies and Gibbs free energies were calculated for all selected drugs. Results:Diazepam induced hypothermia was reversed by flumazenil or picrotoxin. Rats injected with APAP displayed dose- and time-related hypothermia. For combined administration, the hypothermic effect of APAP (200 mg/kg) was strongly reduced by pretreatment with picrotoxin or flumazenil P<0.0001and P<0.01, respectively. Selective structural data, bond length, dihedral angles, and related distance in pharmacophore of APAP and BZDR models were the same. Some significant structural analogues were obtained between these drugs. Conclusion:Results suggest hypothermic action of acetaminophen may be mediate by its effect at GABAA benzodiazepine receptor.
- انتشار مقاله: 01-03-1395
- نویسندگان: Nematollah Ahangar,Zohreh Esam,Ahmadreza Bekhradnia,Mohammad Ali Ebrahimzadeh
- مشاهده
- جایگاه : پژوهشی
- مجله: Addiction and Health
- نوع مقاله: Journal Article
- کلمات کلیدی: Tramadol,Melatonin,oxidative stress,Mitochondria,Apoptosis
- چکیده:
- چکیده انگلیسی: Background: The aim of the present study was to investigate the protective properties of melatonin (MT)
against oxidative stress, mitochondrial dysfunction, and apoptosis induced by tramadol-reproductive toxicity
in male rats.
Methods: The rats were divided into the 7 groups of control, melatonin (1.5 mg/kg), tramadol (50 mg/kg), and
melatonin (1, 1.5 and 2.5 mg/kg) administered 30 minutes before tramadol and vitamin C group (100 mg/kg).
All injections were performed intraperitoneally. After administration for 3 consecutive weeks, the animals were
killed and testis tissues were used for assessment of oxidative stress markers including lipid peroxidation
(LPO), glutathione (GSH) content and protein carbonyl (PrC), and sperm analysis. Mitochondria were isolated
from rat’s testis using differential centrifugation technique and were studied in terms of mitochondrial
viability, mitochondrial membrane potential (MMP), and mitochondrial swelling. The other part of the tissue
sample was placed in RNA protector solution for assessment of Bax and Bcl-2 gene expression through realtime polymerase chain reaction (real-time PCR) assay.
Findings: Tramadol caused a significant decline in epidermal sperm count, motility, and morphology, as well
as a significant decrease in GSH level and mitochondrial function, and a significant evaluation of LPO, PrC,
MMP, and mitochondrial swelling. In addition, tramadol induced a significant decrease in Bcl-2 gene
expression, and increase in Bax gene expression. However, pretreatment of rats with MT improved sperm
analysis, and testicular antioxidative status, and mitochondrial function. Furthermore, MT pretreatment
regulated testicular Bcl-2 and Bax expressions.
Conclusion: Considering the protective effects of MT against reproductive toxicity induced by tramadol, this
compound can be used as a possible agent for the prevention and treatment of tramadol-induced reproductive
toxicity.
- انتشار مقاله: 11-04-1399
- نویسندگان: Motahareh Koohsari,Nematollah Ahangar,Ebrahim Mohammadi,Fatemeh Shaki
- مشاهده