1.Significance of Attending to Instrument Planning and Validation Stages in Nursing Discipline.
Maryam ESMAEILI ; Nahid DEHGHAN-NAYERI
Asian Nursing Research 2012;6(2):82-83
No abstract available.
2.The ability of orexin-A to modify pain-induced cyclooxygenase-2and brain-derived neurotrophic factor expression is associated with its ability to inhibit capsaicin-induced pulpal nociception in rats
Fatemeh SHAHSAVARI ; Mehdi ABBASNEJAD ; Saeed ESMAEILI-MAHANI ; Maryam RAOOF
The Korean Journal of Pain 2022;35(3):261-270
Background:
The rostral ventromedial medulla (RVM) is a critical region for the management of nociception. The RVM is also involved in learning and memory processes due to its relationship with the hippocampus. The purpose of the present study was to investigate the molecular mechanisms behind orexin-A signaling in the RVM and hippocampus’s effects on capsaicin-induced pulpal nociception and cog-nitive impairments in rats.
Methods:
Capsaicin (100 g) was applied intradentally to male Wistar rats to induce inflammatory pulpal nociception. Orexin-A and an orexin-1 receptor antagonist (SB-334867) were then microinjected into the RVM. Immunoblotting and immunofluorescence staining were used to check the levels of cyclooxygenase-2 (COX-2) and brain-derived neurotrophic factor (BDNF) in the RVM and hippocampus.
Results:
Interdental capsaicin treatment resulted in nociceptive responses as well as a reduction in spatial learning and memory. Additionally, it resulted in decreased BDNF and increased COX-2 expression levels. Orexin-A administration (50 pmol/1 μL/rat) could reverse such molecular changes. SB-334867 microinjection (80 nM/1 μL/rat) suppressed orexin’s effects.
Conclusions
Orexin-A signaling in the RVM and hippocampus modulates capsaicininduced pulpal nociception in male rats by increasing BDNF expression and decreasing COX-2 expression.
3.Orexin-A inhibits capsaicin-induced changes in cyclooxygenase-2 and brain-derived neurotrophic factor expression in trigeminal nucleus caudalis of rats
Razieh KOOSHKI ; Mehdi ABBASNEJAD ; Saeed ESMAEILI MAHANI ; Maryam RAOOF ; Mohammad Mehdi MOEINI AGHTAEI ; Shahriar DABIRI
The Korean Journal of Pain 2018;31(3):174-182
BACKGROUND: The trigeminal nucleus caudalis (Vc) is a primary central site for trigeminal transmitting. Noxious stimulation of the trigeminal nociceptors alters the central synaptic releases and neural expression of some inflammatory and trophic agents. Orexin-A and the orexin 1 receptor (OX1R) are expressed in pain pathways including trigeminal pain transmission. However, the the mechanism(s) underling orexin-A effects on trigeminal pain modulation have not been fully clarified. METHODS: Trigeminal pain was induced by subcutaneous injection of capsaicin in the upper lip in rats. The effect of trigeminal pain on cyclooxygenase-2 (COX-2) and brain-derived neurotrophic factor (BDNF) expression in the Vc of animals was determined by immunofluorescence. Subsequently, OX1R agonist (orexin-A) and antagonist (SB-334867-A) was administrated in the Vc to investigate the possible roles of the Vc OX1R on changes in COX-2 and BDNF levels following pain induction. RESULTS: The data indicated an increase in COX-2 and decrease in BDNF immuno-reactivity in the Vc of capsaicin, and capsaicin- pretreated with SB-334867-A (80 nM), groups of rat. However, the effect of capsaicin on COX-2 and BDNF expressions was reversed by a Vc microinjection of orexin-A (100 pM). CONCLUSIONS: Overall, the present data reveals that orexin-A can attenuate capsaicin-induced trigeminal pain through the modulation of pain effects on COX-2 and BDNF expressions in the Vc of rats.
Animals
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Brain-Derived Neurotrophic Factor
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Capsaicin
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Cyclooxygenase 2
;
Facial Pain
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Fluorescent Antibody Technique
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Injections, Subcutaneous
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Lip
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Microinjections
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Nociceptors
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Orexin Receptor Antagonists
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Orexins
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Pain Measurement
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Pain Perception
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Rats
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Trigeminal Caudal Nucleus
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Trigeminal Neuralgia
;
Trigeminal Nuclei
4.The role of basolateral amygdala orexin 1 receptors on the modulation of pain and psychosocial deficits in nitroglycerin-induced migraine model in adult male rats
Khadijeh ASKARI-ZAHABI ; Mehdi ABBASNEJAD ; Razieh KOOSHKI ; Maryam RAOOF ; Saeed ESMAEILI-MAHANI ; Ali Mohammad POURRAHIMI ; Mahnaz ZAMYAD
The Korean Journal of Pain 2022;35(1):22-32
Background:
Migraine headaches have been associated with sensory hyperactivity and anomalies in social/emotional responses. The main objective of this study was to evaluate the potential involvement of orexin 1 receptors (Orx1R) within the basolateral amygdala (BLA) in the modulation of pain and psychosocial dysfunction in a nitroglycerin (NTG)-induced rat model of migraine.
Methods:
Adult male Wistar rats were injected with NTG (5 mg/kg, intraperitoneal) every second day over nine days to induce migraine. The experiments were done in the following six groups (6 rats per group): untreated control, NTG, NTG plus vehicle, and NTG groups that were post-treated with intra-BLA microinjection of Orx1R antagonist SB-334867 (10, 20, and 40 nM). Thermal hyperalgesia was assessed using the hot plate and tail-flick tests. Moreover, the elevated plus maze (EPM) and open field (OF) tests were used to assess anxiety-like behaviors. The animals’ sociability was evaluated using the three-chamber social task. The NTG-induced photophobia was assessed using a light-dark box.
Results:
We observed no change in NTG-induced thermal hyperalgesia following administration of SB-334867 (10, 20, and 40 nM). However, SB-334867 (20 and 40 nM) aggravated the NTG-induced anxiogenic responses in both the EPM and OF tasks. The NTG-induced social impairment was overpowered by SB-334867 at all doses. Time spent in the dark chamber of light-dark box was significantly increased in rats treated with SB-334867 (20 and 40 nM/rat).
Conclusions
The findings suggest a role for Orx1R within the BLA in control comorbid affective complaints with migraine in rats.
5.Indigenous microbiota protects development of medication-related osteonecrosis induced by periapical disease in mice.
Wen DU ; Mengyu YANG ; Terresa KIM ; Sol KIM ; Drake W WILLIAMS ; Maryam ESMAEILI ; Christine HONG ; Ki-Hyuk SHIN ; Mo K KANG ; No-Hee PARK ; Reuben H KIM
International Journal of Oral Science 2022;14(1):16-16
Bacterial infection is a common finding in patients, who develop medication-related osteonecrosis of the jaw (MRONJ) by the long-term and/or high-dose use of anti-resorptive agents such as bisphosphonate (BPs). However, pathological role of bacteria in MRONJ development at the early stage remains controversial. Here, we demonstrated that commensal microbiota protects against MRONJ development in the pulp-exposed periapical periodontitis mouse model. C57/BL6 female mice were treated with intragastric broad-spectrum antibiotics for 1 week. Zoledronic acid (ZOL) through intravenous injection and antibiotics in drinking water were administered for throughout the experiment. Pulp was exposed on the left maxillary first molar, then the mice were left for 5 weeks after which bilateral maxillary first molar was extracted and mice were left for additional 3 weeks to heal. All mice were harvested, and cecum, maxilla, and femurs were collected. ONJ development was assessed using μCT and histologic analyses. When antibiotic was treated in mice, these mice had no weight changes, but developed significantly enlarged ceca compared to the control group (CTL mice). Periapical bone resorption prior to the tooth extraction was similarly prevented when treated with antibiotics, which was confirmed by decreased osteoclasts and inflammation. ZOL treatment with pulp exposure significantly increased bone necrosis as determined by empty lacunae and necrotic bone amount. Furthermore, antibiotics treatment could further exacerbate bone necrosis, with increased osteoclast number. Our findings suggest that the commensal microbiome may play protective role, rather than pathological role, in the early stages of MRONJ development.
Animals
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Bisphosphonate-Associated Osteonecrosis of the Jaw/prevention & control*
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Bone Density Conservation Agents
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Diphosphonates
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Female
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Humans
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Mice
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Microbiota
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Periapical Diseases
;
Zoledronic Acid