Physiology
Sina Tamaddonfard; Amir Erfanparast; Esmaeal Tamaddonfard; Farhad Soltanalinejad
Volume 15, Issue 1 , January 2024, , Pages 35-41
Abstract
Neuroprotective effects for natural products are supported by several studies. In this regard, safranal, a constitute of saffron, has the potential to exert beneficial effects in neurological disorders such as Parkinson's disease, epilepsy, stroke, multiple sclerosis and Alzheimer's disease. Here, we ...
Read More
Neuroprotective effects for natural products are supported by several studies. In this regard, safranal, a constitute of saffron, has the potential to exert beneficial effects in neurological disorders such as Parkinson's disease, epilepsy, stroke, multiple sclerosis and Alzheimer's disease. Here, we investigated the effect of safranal on penicillin-induced epileptiform activity. Also, the effects of intracerebroventricular (ICV) microinjection of AM251 as a CB1-cannabinoid receptors antagonist to clarify the possible mechanism of safranal were evaluated. Epileptiform activity was induced by intra-cortical administration of penicillin (300 IU, 1.50 μL) in urethane-anesthetized rats. Electrocorticographic recordings were used to analyze the frequency and amplitude of spike waves. Intraperitoneal injections of safranal at doses of 1.00 and 4.00 mg kg-1 significantly reduced both the number and amplitude of spike waves. The ICV microinjection of AM251 (0.50 μg 2.00 μL-1) significantly increased the frequency and amplitude of spike waves. In addition, the anti-epileptic effect induced by administration of safranal at a dose of 4.00 mg kg-1 was partially prevented by ICV microinjection of 0.50 μg 2.00 μL-1 of AM251. The results showed anti-epileptiform activities for safranal. Central CB1 cannabinergic receptors might be involved in the anti-epileptiform activity of safranal.
Pathology
Sadat Ghafarzadeh; Rahim Hobbenaghi; Esmaeal Tamaddonfard; Amir Abbas Farshid; Mehdi Imani
Volume 10, Issue 4 , December 2019, , Pages 277-284
Abstract
Crocin is a plant-derived carotenoid and bears potent antioxidant property. Ranitidine (a histamine H2 receptor blocker) is used for peptic ulcer treatment. The present study was planned to investigate the effects of crocin and ranitidine on indomethacin-induced ulcer in small intestine of rats. Animals ...
Read More
Crocin is a plant-derived carotenoid and bears potent antioxidant property. Ranitidine (a histamine H2 receptor blocker) is used for peptic ulcer treatment. The present study was planned to investigate the effects of crocin and ranitidine on indomethacin-induced ulcer in small intestine of rats. Animals were randomized into two major groups including indo-methacin (10.00 mg kg-1, ulcer group, 48 rats) and normal saline (1.00 mL kg-1, intact group, 48 rats) groups. Each of these two major groups was subdivided into eight subgroups for intra-peritoneal (IP) injections of normal saline, crocin (2.50, 10.00 and 40.00 mg kg-1), ranitidine (5.00 and 20.00 mg kg-1), crocin (2.50 and 10.00 mg kg-1) plus ranitidine (5.00 mg kg-1). Indomethacin induced intestinal ulcer was characterized by bleeding, inflammation, epithelial hyperplasia and crypt loss. This non-steroidal anti-inflammatory drug (NSAID), indomethacin decreased goblet cell number and superoxide dismutase (SOD) activity and increased small intestine weight, organo-somatic index (OSI), malodealdehyde (MDA), tumor necrosis factor-α (TNF-α) and caspase-3 contents of intestine. Crocin resolved all the above-mentioned parameter changes induced by indomethacin. These treatments produced no significant effects on the above-mentioned parameters of intact group. The results of the present study showed tissue protective and anti-ulcer effects of crocin on small intestine by antioxidant, anti-inflammatory and anti-apoptotic mechanisms. Ranitidine alone showed no effect; however, in combination with crocin it exerted recovery effects. It is recommended that crocin, be considered as a therapeutic agent for NSAIDs-induced intestinal damage management.
Physiology
Esmaeal Tamaddonfard; Sina Tamaddonfard; Siamak Cheraghiyan
Volume 9, Issue 4 , December 2018, , Pages 329-335
Abstract
Vitamin B12 modulates pain at the local and peripheral levels. This study has investigated the effects of intracerebroventricular (ICV) injection of vitamin B12 on themuscle pain. We used diclofenac (cyclooxygenase inhibitor) and naloxone (opioid receptors antagonist) to clarify the possible mechanisms. ...
Read More
Vitamin B12 modulates pain at the local and peripheral levels. This study has investigated the effects of intracerebroventricular (ICV) injection of vitamin B12 on themuscle pain. We used diclofenac (cyclooxygenase inhibitor) and naloxone (opioid receptors antagonist) to clarify the possible mechanisms. For ICV injections, a guide cannula was implanted in the left lateral ventricle of the brain. Muscle pain was induced by intramuscular injection of formalin (2.50%; 50 µl) in the right gastrocnemius muscle and the number of paw flinching was recorded at 5-min blocks for 60 min. Locomotor activity was performed using an open-field test. Formalin induced a biphasic pain. Vitamin B12 (1.25, 2.50, 5.00 and 10.00 µg per rat) and diclofenac (12.50 and 25.00 µg per rat) significantly reduced both phases pain intensity. Significant antinociceptive effects were observed after combined treatments of diclofenac (6.25 and 12.50 µg per rat) with vitamin B12 (0.63 and 2.50 µg per rat), respectively. Prior ICV injection of naloxone (10.00 µg per rat) prevented vitamin B12 (10.00 µg per rat) and diclofenac (25.00 µg per rat) induced antinociceptive effects. All the above-mentioned chemicals did not alter locomotor behavior in an open-field test. The present results showed that the cyclooxygenase pathway and opioid receptors may be involved in the central antinociceptive effect of vitamin B12. In addition, opioid receptors might be involved in diclofenac-induced antinociception.
Physiology
Esmaeal Tamaddonfard; Amir Erfanparast
Volume 8, Issue 1 , March 2017, , Pages 29-34
Abstract
The parafascicular nucleus (PFN) of thalamus, as a supraspinal structure, has an important role in processing of nociceptive information. In addition, μ-opioid receptor contributes to supraspinal modulation of nociception. In the present study, the effects of microinjection of naloxone (a non-specific ...
Read More
The parafascicular nucleus (PFN) of thalamus, as a supraspinal structure, has an important role in processing of nociceptive information. In addition, μ-opioid receptor contributes to supraspinal modulation of nociception. In the present study, the effects of microinjection of naloxone (a non-specific opioid-receptor antagonist) and naloxonazine (a specific μ-opioid receptor antagonist) were investigated on morphine-induced antinociception in a rat model of acute trigeminal pain. Right and left sides of PFN of thalamus were implanted with two guide cannulas. Acute trigeminal pain was induced by local corneal surface application of hypertonic saline and the number of eye wipes as a pain index was recorded for 30 sec. Microinjection of morphine at doses of 1, 2 and 4 μg per site significantly (p < 0.05) decreased the number of eye wipes. Alone microinjection of naloxone (4 μg per site) and naloxonazine (1 and 2 μg per site) significantly (p < 0.05) increased corneal pain severity. Prior microinjection of naloxone (2 and 4 μg per site) and naloxonazine (1 and 2 μg per site) significantly (p < 0.05) prevented the antinociceptive effect induced by morphine (4 μg per site). All the above-mentioned chemicals did not alter locomotor behavior in an open-field test. The results of the present study showed an antinociceptive effect of morphine at the PFN level of thalamus. Mu-opioid receptor of the PFN of thalamus may be involved in morphine-induced antinociception.
Esmaeal Tamaddonfard1; Farzad Samadi; Karim Egdami
Volume 4, Issue 1 , March 2013, , Pages 19-24
Abstract
The present study was performed to investigate the effects of long-term intraperitoneal (IP) injection of vitamin B12 and diclofenac in separate and combined treatments on cold and mechanical allodynia in a neuropathic pain model in rats. Neuropathic pain was induced by crush injury in right tibial nerve. ...
Read More
The present study was performed to investigate the effects of long-term intraperitoneal (IP) injection of vitamin B12 and diclofenac in separate and combined treatments on cold and mechanical allodynia in a neuropathic pain model in rats. Neuropathic pain was induced by crush injury in right tibial nerve. Acetone spray and von Frey tests were used to obtain cold and mechanical allodynia responses, respectively, on day 11 after nerve crush. Normal saline, vitamin B12 and diclofenac were injected intraperitoneally for 10 consecutive days after surgery. Normal saline treated rats showed cold and mechanical allodynia responses after nerve crush. Vitamin B12 at doses of 50, 100 and 200 µg kg-1 and diclofenac at a dose of 2 mg kg-1 produced antiallodynic effects. Antiallodynic effects were not observed when subanalgesic doses of vitamin B12 (25 µg kg-1) and diclofenac (0.25 mg kg-1) were used together. By increasing the dose of vitamin B12 to an effective dose (100 µg kg-1), antiallodynic effects were observed when compared with diclofenac (0.25 mg kg-1) alone. The results indicated that vitamin B12 and diclofenac produced neuropathic pain suppressing effects. Moreover, a potentiation effect was observed between vitamin B12 and diclofenac.