این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
Acta Medica Iranica، جلد ۵۶، شماره ۸، صفحات ۴۹۸-۵۰۷
عنوان فارسی
چکیده فارسی مقاله
کلیدواژه‌های فارسی مقاله
عنوان انگلیسی Pharmacological Profile for the Contribution of NO/cGMP Pathway on Chlorpheniramine Antidepressant-Like Effect in Mice Forced Swim Test
چکیده انگلیسی مقاله Chlorpheniramine, a first-generation antihistamine, is widely used for allergic reactions. Previous studies showed the interaction between antidepressant activity and nitric oxide and cyclic guanosine monophosphate (NO/cGMP) pathway. Thus, we aimed to assess the possible involvement of NO/cGMP pathway in this effect using forced swim test (FST) in male mice. To evaluate the locomotor activity and immobility time, we performed open field test (OFT) and FST on each mouse. Chlorpheniramine was administered intraperitoneally (i.p.) (0.1, 0.3, 1, 10 mg/kg) 30 minutes before FST. To assess the involvement of NO/cGMP pathway, a non-selective nitric oxide synthase (NOS) inhibitor, L-NAME (10mg/kg, i.p.), a selective inducible NOS (iNOS) inhibitor, aminoguanidine (50 mg/kg, i.p.), a selective neural NOS (nNOS) inhibitor, 7-nitroindazole (7-NI, 30 mg/kg, i.p.), a NO precursor, L-arginine (750 mg/kg, i.p.) and a selective phosphodiesterase-5 (PDE-5) inhibitor, sildenafil (5 mg/kg, i.p.) was co-administered with chlorpheniramine. Chlorpheniramine significantly decreased the immobility time at doses of 1mg/kg ( P < 0. 01) and 10 mg/kg ( P < 0.001). Administration of L-NAME ( P < 0.01) and 7-NI enhanced the anti-immobility activity of chlorpheniramine ( P < 0.001), while aminoguanidine did not have any significant effects on the immobility time ( P >0.05). Moreover, pretreatment with L-arginine ( P < 0.01) and sildenafil ( P < 0.001) significantly reduced the anti-immobility effect of chlorpheniramine. These treatments did not alter the locomotor activity of mice in OFT. Our results revealed that the antidepressant-like effect of chlorpheniramine is mediated through inhibition of NO/cGMP pathway.
کلیدواژه‌های انگلیسی مقاله
نویسندگان مقاله | Saeed Shakiba
Departments of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.


| Nazanin Rajai
Departments of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.


| Mehdi Qaempanah
Departments of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.


| Nazgol‐Sadat Haddadi
Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.


| Abbas Norouzi-Javidan
Departments of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.


| Reyhaneh Akbarian
Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. AND Departments of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.


| Sattar Ostadhadi
Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. AND Departments of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran.


| Ahmad-Reza Dehpour


نشانی اینترنتی http://acta.tums.ac.ir/index.php/acta/article/view/6933
فایل مقاله اشکال در دسترسی به فایل - ./files/site1/rds_journals/56/article-56-1062150.pdf
کد مقاله (doi)
زبان مقاله منتشر شده en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده Articles
برگشت به: صفحه اول پایگاه   |   نسخه مرتبط   |   نشریه مرتبط   |   فهرست نشریات