• International Journal of Oral Biology
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• v.35 no.3
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• pp.75-81
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• 2010

The present study investigated the role of ERK in the onset of mechanical and cold allodynia in a rat model of compression of the trigeminal ganglion by examining changes in the air-puff thresholds and number of scratches following the intracisternal injection of PD98059, a MEK inhibitor. Male Sprague Dawley rats weighing between 250 and 260 g were used. Under anesthesia, the rats were mounted onto a stereotaxic frame and received 4% agar ($10\;{\mu}l$) solution to compress the trigeminal ganglion. In the control group, the animals were given a sham operation without the application of agar. Changes in behavior were examined at 3 days before and at 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Compression of the trigeminal ganglion significantly decreased the air-puff thresholds. Mechanical allodynia was established within 3 days and persisted over postoperative day 24. To evaluate cold allodynia, nociceptive scratching behavior was monitored after acetone application on the vibrissa pad of the rats. Compression of the trigeminal ganglion was found to produce significant cold allodynia, which persisted for more than 40 days after surgery. On postoperative day 14, the intracisternal administration of $1\;{\mu}g$ or $10\;{\mu}g$ of PD98059 in the rat model significantly decreased the air-puff thresholds on both the ipsilateral and contralateral side. The intracisternal administration of $10\;{\mu}g$ of PD98059 also significantly alleviated the cold allodynia, compared with the vehicle-treated group. These results suggest that central ERK plays an important role in the development of mechanical and cold allodynia in rats with compression of the trigeminal ganglion and that a targeted blockade of this pathway is a potential future treatment strategy for trigeminal neuralgia-like nociception.

• Korean Journal of Pharmacognosy
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• v.51 no.1
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• pp.41-48
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• 2020

This study was conducted to evaluate the effects of Padina arborescens and 1-O-myristoyl-2-O-oleoyl-3-O-(α-D-glucopyranosyl)-glycerol(MOGG), its active component, on the prevention of hair loss. The P. arborescens extract and MOGG inhibited the activity of 5α-reductase, which converts testosterone to dihydrotestosterone(DHT), a main cause of androgenetic alopecia. When immortalized rat vibrissa dermal papilla cells were treated with MOGG, the proliferation of dermal papilla cells significantly increased. In addition, we found that the P. arborescens extract and MOGG could open the K_ATP channel, which may contribute to increase hair growth. Furthermore, MOGG promoted PGE₂ production in HaCaT cells. The results suggest that MOGG from the P. arborescens extract has the potential to treat alopecia via 5α-reductase inhibition, the proliferation of dermal papilla, the opening of the K_ATP channel and/or increase of PGE₂ production.

• Journal of the korean academy of Pediatric Dentistry
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• v.23 no.3
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• pp.582-592
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• 1996

본 실험은 삼차신경 자극으로 발생되는 체성 감각 유발 전위에 대한 국소마취제의 효과를 관찰하였다. 나트륨 통로차단을 통하여 약리작용을 나타내는 것으로 알려져 있는 리도카인를 뇌 피질에 국소 투여한 후 삼차신경의 체성 감각유발 전위의 강도및 지연시간을 측정하였다. 케타민으로 마취된 흰쥐의 대측성 구레나룻 자극후 뇌의 체성 감각영역으로부터 기록되는 유발전위를 분석한 결과, 리도카인을 뇌 피질에 국소 투여시 유발전위의 강도 및 지연시간의 감소가 나타났으며, 필드 전위의 형태는 이상성 (양극성 및 음극성) 혹은 삼상성 (양극성, 음극성 및 양극성) 의 파형으로 나타났다. 필드 전위의 발생 부위는 뇌 피질의 중대뇌동맥의 상행지 상방영역이었다. 본 실험에서 나타난 초기 전위변동은 피질판 상층에 존재하는 신경세포의 탈분극 과청에 의하여 생성되고 후기의 전위 변동은 동일 영역의 하층 신경세포에서 과분극 혹은 재분극이 발생한 결과라고 유추된다. 따라서 삼차신경계의 체성 감각 영역에서는 피질 상층및 하층의 과립성 피라미드 세포의 순차적인 활성화에 의하여 기본적인 신경 회로망이 형성되어 있으며 생리적 자극으로 유발되는 필드 전위는 이러한 신경망를 통하여 발생될 것으로 사료된다.

• International Journal of Oral Biology
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• v.33 no.4
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• pp.155-162
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• 2008

The present study investigated inflammatory hypersensitivity following compression of the trigeminal ganglion in rats. Experiments were carried out on male Sprague-Dawley rats weighing 250-260 g. Under anesthesia, rats were mounted on a stereotaxic frame and injected with $8{\mu}L$ of 4% agar solution through a stainless steel injector to compress the trigeminal ganglion. In the control group, rats underwent a sham operation without agar injection. Injection sites were examined with a light micrograph after compression of the trigeminal ganglion. Air-puff thresholds (mechanical allodynia) were evaluated 3 days before surgery and 3, 7, 10, 14, 17, 21, 24, 30, and 40 days after surgery. Air-puff thresholds significantly decreased after compression of the trigeminal ganglion. Mechanical allodynia was established within 3 days and remained strong over 24 days, returning to preoperative levels approximately 40 days following compression. After subcutaneous injection of 5% formalin ($50{\mu}L$) in the compression of the trigeminal ganglion-treated rats, nociceptive scratching behavior was recorded for 9 successive 5-min internals. Injection of formalin into the vibrissa pad significantly increased the number of scratches and duration of noxious behavioral responses in sham-treated rats. Noxious behavioral responses induced by subcutaneous formalin administration were significantly potentiated in rats with trigeminal ganglion compression. These findings suggest that compression of the trigeminal ganglion enhanced formalin-induced infla-mmatory pain in the orofacial area.

• Biomolecules & Therapeutics
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• v.20 no.1
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• pp.118-124
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• 2012

This study was conducted to evaluate the effect of Grateloupia elliptica, a seaweed native to Jeju Island, Korea, on the prevention of hair loss. When immortalized rat vibrissa dermal papilla cells were treated with extract of G. elliptica, the proliferation of dermal papilla cells significantly increased. In addition, the G. elliptica extract significantly inhibited the activity of $5{\alpha}$-reductase, which converts testosterone to dihydrotestosterone (DHT), a main cause of androgenetic alopecia. On the other hand, the G. elliptica extract promoted $PGE_2$ production in HaCaT cells in a dose-dependent manner. The G. elliptica extract exhibited particularly high inhibitory effect on LPS-stimulated IL-12, IL-6, and TNF-${\alpha}$ production in lipopolysaccharide (LPS)-stimulated bone marrow-derived dendritic cells. The G. elliptica extract also showed inhibitory activity against Pityrosporum ovale, a main cause of dandruff. These results suggest that G. elliptica extract has the potential to treat alopecia via the proliferation of dermal papilla, $5{\alpha}$-reductase inhibition, increase of $PGE_2$ production, decrease of LPS-stimulated pro-inflammatory cytokines and inhibitory activity against Pityrosporum ovale.

• International Journal of Oral Biology
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• v.36 no.3
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• pp.143-148
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• 2011

The present study investigated the role of peripheral P2X receptors in inflammatory pain transmission in the orofacial area in rats. Experiments were carried out on male Sprague-Dawley rats weighing 220 to 280 g. Formalin (5%, 50 ${\mu}L$) and complete Freund's adjuvant (CFA, 25 ${\mu}L$) was applied subcutaneously to the vibrissa pad to produce inflammatory pain. TNP-ATP, a $P2X_{2,2/3,4}$ receptor antagonist, or OX-ATP, a $P2X_7$ receptor antagonist, was then injected subcutaneously at 20 minutes prior to formalin injection. One of the antagonists was administered subcutaneously at three days after CFA injection. The subcutaneous injection of formalin produced a biphasic nociceptive behavioral response. Subcutaneous pretreatment with TNP-ATP (80, 160 or 240 ${\mu}g$) significantly suppressed the number of scratches in the second phase produced by formalin injection. The subcutaneous injection of 50 ${\mu}g$ of OX-ATP also produced significant antinociceptive effects in the second phase. Subcutaneous injections of CFA produced increases in mechanical and thermal hypersensitivity. Both TNP-ATP (480 ${\mu}g$) and OX-ATP (100 ${\mu}g$) produced an attenuation of mechanical hypersensitivity. However, no change was observed in thermal hypersensitivity after the injection of either chemical. These results suggest that the blockade of peripheral P2X receptors is a potential therapeutic approach to the onset of inflammatory pain in the orofacial area.

• International Journal of Oral Biology
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• v.36 no.2
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• pp.43-50
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• 2011

Voltage dependent calcium channel (VDCC), one of the most important regulator of $Ca^{2+}$ concentration in neuron, play an essential role in the central processing of nociceptive information. The present study investigated the antinociceptive effects of L, T or N type VDCC blockers on the formalin-induced orofacial inflammatory pain. Experiments were carried out on adult male Sprague-Dawley rats weighing 220-280 g. Anesthetized rats were individually fixed on a stereotaxic frame and a polyethylene (PE) tube was implanted for intracisternal injection. After 72 hours, 5% formalin ($50 \;{\mu}L$) was applied subcutaneously to the vibrissa pad and nociceptive scratching behavior was recorded for nine successive 5 min intervals. VDCC blockers were administered intracisternally 20 minutes prior to subcutaneous injection of formalin into the orofacial area. The intracisternal administration of 350 or $700{\mu}g$ of verapamil, a blocker of L type VDCC, significantly decreased the number of scratches and duration in the behavioral responses produced by formalin injection. Intracisternal administration of 75 or $150 \;{\mu}g$ of mibefradil, a T type VDCC blocker, or 11 or $22\; {\mu}g$ of cilnidipine, a N type VDCC blocker, also produced significant suppression of the number of scratches and duration of scratching in the first and second phase. Neither intracisternal administration of all VDCC blockers nor vehicle did not affect in motor dysfunction. The present results suggest that central VDCCs play an important role in orofacial nociceptive transmission and a targeted inhibition of the VDCCs is a potentially important treatment approach for inflammatory pain originating in the orofacial area.

• Biomedical Science Letters
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• v.24 no.3
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• pp.239-244
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• 2018

Recently, many researches regarding the natural products which alternate with chemical products have been done. Among them, boswellia is well known for effect on anti-oxidative effect and inflammation. The aim was the effect boswellia of formalin- induced orofacial and temporomandibular joint (TMJ) pain on experimental animals was investigated. Experiments were carried out using subcutaneous (SC) pain model and TMJ pain model that were induced by the injection of 5% formalin into the right vibrissa pad (SC, $50{\mu}L$) or TMJ ($30{\mu}L$) of rats, respectively. In both models, formalin (5%), formalin after distilled water (vehicle), formalin after boswellia extract (p.o., concentrations of 15, 30 mg/kg) (n=6). The number of scratching on the injected region was scored during the 9 successive periods of 5 min intervals following injection of formalin. Oral administration of boswellia (15, 30 mg / kg) reduced formalin-induced SC orofacial pain behavioral responses. SC orofacial pain behavioral responses was significantly reduced at 20~35 min. In the experimental group injected into temporomandibular joints, the pain response was significantly reduced by $276.2{\pm}8.20$ and $78.3{\pm}4.7$ after oral administration of boswellia (15, 30 mg / kg) at $398.3{\pm}24.8$ times. As a result of the passage of time, the oral administration of boswellia showed a significant effect of reducing the temporomandibular joint pain 30 minutes after the injection of formalin. This study confirmed that oral administration of boswellia modulated the pain behavior in both models. In conclusion, boswellia extract may be a potential therapeutic treatment for orofacial pain.

• International Journal of Oral Biology
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• v.40 no.2
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• pp.71-77
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• 2015

The activation of glial cells in the spinal cord has been contribute to the initiation and maintenance of pain facilitation induced by peripheral inflammation and nerve injury. The present study investigated effects of botulinum toxin type A (BoNT-A), injected subcutaneously or intracisternally, on the expression of microglia and astrocytes in rats. Complete Freund's Adjuvant (CFA)-induced inflammation was employed as an orofacial chronic inflammatory pain model. A subcutaneous injection of $40{\mu}L$ CFA into the vibrissa pad was performed under 3% isoflurane anesthesia in SD rats. Immunohistochemical analysis for changes in Iba1 (a microglia marker) and GFAP (an astrocyte marker), were performed 5 days after CFA injection. Subcutaneous injection of CFA produced increases in Iba1 and GFAP expression, in the ipsilateral superficial lamia I and II in the medullary dorsal horn of rats. Subcutaneous treatment with BoNT-A attenuated the up-regulation of Iba1 and GFAP expressions induced by CFA injection. Moreover, intracisternal injection of BoNT-A also attenuated the up-regulated Iba1 and GFAP expressions. These results suggest that the anti-nociceptive action of BoNT-A is mediated by modulation activation of glial cells, including microglia and astrocyte.

• International Journal of Oral Biology
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• v.42 no.1
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• pp.1-8
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• 2017

In the present study, we investigated the role of peripheral ionotropic receptors in artemin-induced thermal hyperalgesia in the orofacial area. Male Sprague-Dawley rats weighting 230 to 280 g were used in the study. Under anesthesia, a polyethylene tube was implanted in the subcutaneous area of the vibrissa pad, which enabled drug-injection. After subcutaneous injection of artemin, changes in air-puff thresholds and head withdrawal latency time were evaluated. Subcutaneous injection of artemin (0.5 or $1{\mu}g$) produced significant thermal hyperalgesia in a dose-dependent manner. However, subcutaneous injection of artemin showed no effect on air-puff thresholds. IRTX ($4{\mu}g$), a TRPV1 receptor antagonist, D-AP5 (40 or $80{\mu}g$), an NMDA receptor antagonist, or NBQX (20 or $40{\mu}g$), an AMPA receptor antagonist, was injected subcutaneously 10 min prior to the artemin injection. Pretreatment with IRTX and D-AP5 significantly inhibited the artemin-induced thermal hyperalgesia. In contrast, pretreatment with both doses of NBQX showed no effect on artemin-induced thermal hyperalgesia. Moreover, pretreatment with H-89, a PKA inhibitor, and chelerythrine, a PKC inhibitor, decreased the artemin-induced thermal hyperalgesia. These results suggested that artemin-induced thermal hyperalgesia is mediated by the sensitized peripheral TRPV1 and NMDA receptor via activation of protein kinases.