• Journal of Acupuncture Research
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• v.22 no.3
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• pp.113-122
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• 2005

Objective : The present study was carried out to investigate the preventive effect of Several Herb - Combined Prescription (SHP) on streptozotocin (STZ) - induced diabetes mellitus. Methods : SHP was given to mice with the combination of oral administration and herbal-acupuncture stimulation. Experimental diabetes was induced by the injection of STZ(50mg/kg) to the rat via the peritoneum The effect of SHP on STZ-induced diabetes was observed by measuring the serum level of insulin, glucose, triglyceride, total cholesterol and lipid peroxides. Hepatic activities of catalase and reduced glutathione were examined. Results : SHP treatment protected them from the hyperglycemia. STZ induced increase of serum triglyceride lowered by SHP treatment. Conclusions : The SHP treatment showed protective effect on diabetic mouse model, and action mechanism of the effect was thought to be concerned with anti-oxidative stress.

• Journal of Acupuncture Research
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• v.22 no.1
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• pp.1-11
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• 2005

Objective : The present study was carried out to investigate the preventive effect of Several Herb-combind Prescription(SHP) on Streptozotocin (STZ) -induced Diabetes mellitus. Methods : SHP was given to rats with the combination of oral administration and herbal-acupuncture stimulation. The experimental animals were divided into 3 groups : normal group of rats, control group of STZ-induced diabetic rats, sample group with SHP treatment. In vitro test of SHP showed ${\alpha}$-glucosidase inhibition, DPPH radical scavenging activity and inhibition of lipid peroxidation. Experimental diabetes was induced by the injection of STZ(60mg/kg) to the rat via the peritoneum. The effect of SHP on STZ-induced diabetes was observed by measuring the seum level of insulin, glucose, triglyceride, total cholesterol and lipid peroxides. Hepatic activities of catalase and reduced glutathione were examined and insulin granule was observed by immunohistochemical examination. Result : STZ caused hyperglycemia and hypoinsulinemia by a selectively destroying pancreatic ${\beta}$-cell. SHP treatment protected them from the hyperglycemia and hypoinsulinemia. STZ induced increase of serum triglyceride lowered by SHP treatment. And by SHP treatment, pancrease showed a big area with positive immuno-reactivity for presence of insulin with many insulin granules distributed in the ${\beta}$-cells in the islets of Langerhans. Contusions : The SHP treatment showed protective effect on diabetic rat model, and action mechanism of the effect was thought to be concerned with anti-oxidative stress.

• The Korean Journal of Pain
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• v.34 no.2
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• pp.176-184
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• 2021

Background: Diabetes-related neuropathic pain frequently occurs, and the underpinning mechanism remains elusive. The periaqueductal gray (PAG) exhibits descending inhibitory effects on central pain transmission. The current work aimed to examine whether inflammatory cytokines regulate mechanical allodynia and thermal hyperalgesia induced by diabetes through the phosphoinositide 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) pathway in the PAG. Methods: Streptozotocin (STZ) was administered intraperitoneally to mimic allodynia and hyperalgesia evoked by diabetes in rats. Behavioral assays were carried out for determining mechanical pain and thermal hypersensitivity. Immunoblot and ELISA were performed to examine PAG protein amounts of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α), as well as their corresponding receptors in STZ rats, and the expression of PI3K/protein kinase B (Akt)/mTOR signaling effectors. Results: Increased PAG p-PI3K/p-Akt/p-mTOR protein amounts were observed in STZ-induced animals, a PI3K-mTOR pathway inhibition in the PAG attenuated neuropathic pain responses. Moreover, the PAG concentrations of IL-1β, IL-6, and TNF-α and their receptors (namely, IL-1R, IL-6R, and tumor necrosis factor receptor [TNFR] subtype TNFR1, respectively) were increased in the STZ rats. Additionally, inhibiting IL-1R, IL-6R, and TNFR1 ameliorated mechanical allodynia and thermal hyperalgesia in STZ rats, alongside the downregulation of PI3K-mTOR signaling. Conclusions: Overall, the current study suggests that upregulated proinflammatory cytokines and their receptors in the PAG activate PI3K-mTOR signaling, thereby producing a de-inhibition effect on descending pathways in modulating pain transmission, and eventually contributing to neuropathic pain.

• Journal of Periodontal and Implant Science
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• v.47 no.5
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• pp.339-350
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• 2017

Purpose: The purpose of this study was to determine the critical diabetes duration in a streptozotocin (STZ)-induced diabetic rat calvarial defect model for experimentation regarding bone regeneration by evaluating the association between diabetes duration and bone healing capacity through histological and radiographic analyses. Methods: Experimental diabetes was induced in 50 of 60 rats by an STZ injection. The rats were divided into 5 groups, including a control group (group 1), according to diabetes durations of 0, 2, 4, 6, and 8 weeks, respectively. Eighteen rats survived: 4 in group 1, 4 in group 2, 4 in group 3, 5 in group 4, and 1 in group 5. Calvarial defects were created at 0, 2, 4, 6, and 8 weeks after STZ injection in groups 1-5. Cone-beam computed tomography scanning was performed at baseline and at 5 and 7 weeks after surgery. The rats were sacrificed 7 weeks after surgery, followed by histological evaluation. Results: The voxel gray values (VGVs) of group 1 and group 2 increased, whereas the VGVs of group 3 and group 4 decreased starting 5 weeks after surgery, although this trend did not reach statistical significance between groups. On the reconstructed 3-dimensional images and based on an analysis of histological features, groups 1 and 2 showed apparent bone regeneration, while groups 3-5 showed very limited bone regeneration. Conclusions: The critical diabetes duration in an STZ-induced diabetic rat calvarial defect model for experimentation regarding bone regeneration was between 2 and 4 weeks. It is suggested that researchers who use STZ-induced diabetic rats wait for more than 2 weeks following diabetes induction before placing implants or conducting bone regeneration studies to allow definite disturbances in bone healing to emerge.