• Clinical and Experimental Pediatrics
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• 제56권3호
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• pp.116-124
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• 2013

Purpose: Tumor necrosis factor (TNF)-${\alpha}$ is thought to contribute to pulmonary hypertension. We aimed to investigate the effect of infliximab (TNF-${\alpha}$ antagonist) treatment on pathologic findings and gene expression in a monocrotaline-induced pulmonary hypertension rat model. Methods: Six-week-old male Sprague-Dawley rats were allocated to 3 groups: control (C), single subcutaneous injection of normal saline (0.1 mL/kg); monocrotaline (M), single subcutaneous injection of monocrotaline (60 mg/kg); and monocrotaline + infliximab (M+I), single subcutaneous injection of monocrotaline plus single subcutaneous injection of infliximab (5 mg/kg). The rats were sacrificed after 1, 5, 7, 14, or 28 days. We examined changes in pathology and gene expression levels of TNF-${\alpha}$, endothelin-1 (ET-1), endothelin receptor A (ERA), endothelial nitric oxide synthase (eNOS), matrix metalloproteinase (MMP) 2, and tissue inhibitor of matrix metalloproteinase (TIMP). Results: The increase in medial wall thickness of the pulmonary arteriole in the M+I group was significantly lower than that in the M group on day 7 after infliximab treatment (P<0.05). The number of intraacinar muscular arteries in the M+I group was lower than that in the M group on days 14 and 28 (P<0.05). Expression levels of TNF-${\alpha}$, ET-1, ERA, and MMP2 were significantly lower in the M+I group than in the M group on day 5, whereas eNOS and TIMP expressions were late in the M group (day 28). Conclusion: Infliximab administration induced early changes in pathological findings and expression levels of TNF-${\alpha}$, and MMP2 in a monocrotaline-induced pulmonary hypertension rat model.

• Biomolecules & Therapeutics
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• 제1권2호
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• pp.280-283
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• 1993

Single subcutaneous injection to SD rats of both sexes was performed to investigate the acute toxicity of new skin allergy-remedy ointment, Banaron. Banaron is composed of lidocaine hydrochloride, chloro-pheniramine maleate, prednisolone acetate, chlorohexidine hydrochloride, methyl salicylate, 1-menthol and d-camphor. The results were as fellows. $LD_{50}$, /TEX> values of Banaron were 8373.6 mg/kg for male and 8260.1 mg/kg for females. Death occurred within 24 hours after administration at doses up to 6600 mg/kg. The main cause of deaths seemed to be respiratory disturbance. General symptoms decreased of activity and respiratory rate, salivation, tremor and loss of consciousness which were commonly observed by some survived animals and all dead animals. No significant gross findings of internal organs and body weight changes in treatment groups in comparison with these of control group were observed at the maximum dose levels in Banaron.

• Journal of Chest Surgery
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• 제19권1호
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• pp.1-11
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• 1986

Using an experimental model of pulmonary hypertension, the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy were studied. Male Sprague-Dawley rats weighing 200~250 gm were used. For the experimental model of pulmonary hypertension, a group of animal was given by a subcutaneous injection of monocrotaline on a dose of 20mg, 40mg, or 60mg per kg of body weight. After 4 weeks of injection, all animals were sacrificed. Another group of animal was given by a subcutaneous injection of monocrotaline in a dose of 40 mg per kg of body weight. The animals were sacrificed, in which they were kept alive for 1, 2, 3 and 4 weeks, respectively. For the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy, the animals treated with monocrotaline were given daily by an intraperitoneal injection of phenoxybenzamine in a dose of 1.3mg/kg of body weight, and were given propranolol via their drinking water at a concentration of 400mg/liter. The animals were sacrificed after 4 weeks of administration. The hearts and lungs were examined histopathologically and morphometrically. The results obtained were summarized as follows: 1. The rats treated with monocrotaline showed an interstitial pneumonitis, medial thickening of the pulmonary small arteries and hypertrophy of the right ventricular wall. 2. The medial thickening of the pulmonary arteries in rats treated with monocrotaline was due to muscular hypertrophy and hyperplasia, and the right ventricular hypertrophy was due to hypertrophy of cardiac muscles. Both medial thickening of the pulmonary arteries and hypertrophy of right ventricular wall were more marked with time and with dose. 3. The daily intraperitoneal injection of phenoxybenzamine suppressed significantly the percentage medial thickness of pulmonary small arteries and the index of right ventricular hypertrophy in rats given a single subcutaneous injection of monocrotaline, but propranolol has shown no protective effect on the development of medial thickening of pulmonary arteries and right ventricular hypertrophy in treated with monocrotaline. The results described above suggested that monocrotaline is an alkaloid selectively inducing pulmonary hypertension and that a-adrenergic receptor is responsible for the pathogenesis of monocrotaline induced pulmonary hypertension in rat.

• 대한물리치료과학회지
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• 제13권1호
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• pp.7-20
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• 2006

Purpose: This study was to find that what mechanism take effects that was Adjuvant Induced Arthritis in Sprague-Dawley rat and then treated the swimming and low power laser. Methods: Adjuvant Induced Arthritis was induced 24 Sprague-Dawley rat by the subcutaneous injection of a 0.2ml Freund's Complete Adjuvant into the right hind paw and right knee joint. Second injection used of 0.05ml Freund's Complete Adjuvant by same method. Arthritic rat were divided 3 groups; arthritic swimming group, arthritic laser group and case control group. The author performed several experimental tests which were the hind paw thickness, step length, knee joint space, activity of enzyme. Results: Hind paw thickness decreased in swimming and laser group. Left step length and knee joint space increased in swimming and laser. Conclusion: Swimming and low power laser therapy on the Adjuvant Induced Arthritis in rats does effective for the rheumatic arthritis therapy by decrease of hind paw thickness, increase of opposite side step length, increase of activity of albumin and IgG and increase of knee joint space.

• 한국임상수의학회지
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• 제16권1호
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• pp.155-162
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• 1999

This study was performed to assess that clinco-therapeutic effect of natural Italian honeybee (Apis mellifera) venom in adjuvant-induced arthritic rat. Ninety Sprague- Dawley rats of male were injected with complete Freund's adjuvant (CFA). Adjuvant arthritis was produced by a single subcutaneous injection of 1 mg Mycobacterium butyricum suspended in 0.1 ml paraffin oil into the right hindpaw. Righting reflex was uniformly lost and considered to be the point of arthritis development on day 14 after CFA injection. Experimental groups were divided into three groups. When arthritis was developed in the rat hind-paw, tested groups were administrated with prednisolone (10 mg/kg, p.o) and honeybee venom (one bee, s.c) at an interval of two days. Control group was subcutaneously injected with 0.1 ml of physiological saline solution in the rat at an interval of two days. Clinical findings, hematological values and histopathological findings were observed during or after the drugs administration. In tested groups, the development of inflammatory edema and polyarthritis on day 14 after treatment was suppressed. No significant differences of hindpaw edema volume and lameness score between prednisolone and honeybee venom groups were observed during or after therapeutic drugs treatment. WBC counts of prednisolone and honeybee venom treatment groups as compared with the control group were getting remarkably decreased during or after the therapeutic drugs administration(p＜0.01). Erosions of articular cartilage and inflammatory cell infiltrations during or after the therapeutic drugs treatment was effectively suppressed in natural honey venom.

• The Journal of Korean Physical Therapy
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• 제18권3호
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• pp.47-58
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• 2006

Purpose: This study was to find that what mechanism take effects that was Adjuvant Induced Arthritis in Sprague-Dawley rat and then treated the swimming and low power laser. Methods: Adjuvant Induced Arthritis was induced 24 Sprague-Dawley rat by the subcutaneous injection of a 0.2ml Freund's Complete Adjuvant into the right hind paw and right knee joint. Second injection used of 0.05ml Freund's Complete Adjuvant by same method. Arthritic rat were divided 3 groups; arthritic swimming group, arthritic laser group and case control group. The author performed several experimental tests which were the hind paw thickness, step length, knee joint space, activity of enzyme. Results: Hind paw thickness decreased in swimming and laser group. Left step length and knee joint space increased in swimming and laser. Conclusion: Swimming and low power laser therapy on the Adjuvant Induced Arthritis in rats does effective for the rheumatic arthritis therapy by decrease of hind paw thickness, increase of opposite side step length, increase of activity of albumin and IgG and increase of knee joint space.

• The Korean Journal of Pain
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• 제9권2호
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• pp.318-325
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• 1996

Background: Sympathectomy relieves pain in sympathectically maintained pain, and subcutaneous injection of norepinephrine(NE) can rekindle mechanical allodynia. However, the mechanism of rekindling is not clear. The purpose of this study is to investigate which subtype of $\alpha$-adrenoceptor is involved in NE-induced rekindling of mechanical allodynia in sympathectomized neuropathic rats. Methods: Neuropathic injury was produced by tightly ligating the left L5 and L6 spinal nerves of 36 male Sprague-Dawley rats and bilateral lumbar sympathectomy was done at two weeks postoperatively. Starting at 7 days after sympathectomy, rekindling of mechanical allodynia was induced by NE and clonidine injected into the left paw, which was reversed by pretreatment of phentolamine and idazoxan. Mechanical allocynia was quantified by measuring the frequency of foot lifts to two von Frey filaments applied to the paw. Results: All tested rats displayed well-developed signs of mechanical allodynia at the left paw that were abolished by a bilateral lumbar sympathectomy. Subcutaneous (s.c.) injection of NE (0.05 ${\mu}g$) into the affected paw of sympathectomized neuropathic rats rekindled previous mechanical allodynia. These effects could be mimicked by an ${\alpha}_2$-receptor agonist clonidine, but not by an ${\alpha}_1$-receptor agonist phenylephrine. The NE-induced rekindling of mechanical allodynia was significantly reduced by prior s.c. injection of a mixed $\alpha$-receptor antagonist phentolamine (20${\mu}g$) and ${\alpha}_2$-receptor antagonist idazoxan(20${\mu}g$), but not by a ${\alpha}_1$-receptor antagonist terazosin (20${\mu}g$). The pretreatment of idazoxan produced dose-related inhibition of NE-induced rekindling of mechanical allodynia. The rekindling induced by ${\alpha}_2$-receptor agonist clonidine (5${\mu}g$) was also reversed by prior s.c. injection of ${\alpha}_2$-receptor antagonist idazoxan (20${\mu}g$). Conclusion: Subcutaneous injection of NE into the paw of sympathectomized neuropathic rats rekindles mechanical allodynia, which is reversed by an ${\alpha}_2$-, but not by an ${\alpha}_1$-receptor antagonist. Therefore, rekindling of mechanical allodynia in sympathectomized neuropathic rats is mediated by ${\alpha}_2$-adrenoceptor.

• International Journal of Oral Biology
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• 제40권2호
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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.

• 한국환경과학회지
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• 제11권6호
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• pp.583-588
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• 2002

Heavy metals like Mercury and Cadmium cause various kinds of toxicities in the organs of Liver and Kidney. To observe the results of toxicity in the liver, kidney, and serum when the rats were injected subcutaneously with HgCl$_2$ and CdC1$_2$ and sacrificed after 24 hours and 72 hours from the last injection, we measured variation of lipidperoxide values in rat liver homogenate, variation of aspartate aminotransferase and alanine aminotransferase in rat serum. Variation of lipidperoxide values in rat kidney homogenate and variation of BUN in rat serum. It was found that Mercury and Cadmium administered subcutaneously to the skin in the air could cause the damages of liver and kidney.

• Biomolecules & Therapeutics
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• 제2권1호
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• pp.59-64
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• 1994

The water extract of pilose antler of Cervus nippon var. mantchuricus (WEC) was investigated in respect of its effect on ceruloplasmin and $\alpha$$_1$-cysteine protease inhibitor (CPI), which are acute-phase proteins showing increased synthesis following inflammatory stimulus in rat. Ceruloplasmin and CPI were spectrophotometrically determined by the oxidase activity and the inhibitory activity on papain, respectively, and their changes in the concentrations in plasma or serum were examined after oral administration of 0.04% WEC to rats during 7 days following inflammation by subcutaneous injection of turpentine oil or lipopolysaccharide (LPS). WEC suppressed the maximum increases in ceruloplasmin and CPI on the 4th day after injection of turpentine oil, but the suppression in ceruloplasmin was more potent than that in CPI. On inflammation by LPS the suppression of the maximum increase in ceruloplasmin by WEC was found on the 2nd day, but the result was less significant from that obtained by the treatment with turpentine oil. Administration of WEC for at least 4 days was required to suppress the maximum increase in ceruloplasmin due to inflammation by turpentine oil. When WEC was administered to rats after injection of turpentine oil, a high dosage (0.36% of WEC) was requisite for the suppression on the maximum increase in ceruloplasmin.