Objectives : This study aimed to compare the anti-diabetic efficacy of Lycii Radicis Cortex (Lycium chinense Mill.) and Corni Fructus (Cornus officinalis) on streptozotocin (STZ)-induced diabetes in rats. Methods : Male Sprague-Dawley rats were divided into four groups; normal, STZ-control, Lycii Radicis Cortex extract-administrated group (LRC) and Corni Fructus extract-administrated group(CF). Diabetes in rats was induced by intraperitonal injection with streptozotocin (STZ) at doses of, 30 mg/kg (body weight) for 5 days (once per a day). STZ-induced diabetic rats were orally administrated LRC and CF extract daily for 4 weeks at doses of 300 mg/kg. Fasting blood glucose, total cholesterol (TC), triglyceride (TG), blood urea nitrogen (BUN) and creatinine were measured in sera of rats. Histopathological changes of kidney, liver and lung tissues were observed by microscope after H&E staining. Results : There were no differences in body and kidney weights, food intake and water intake in LRC- and CF-administrated groups compared with STZ control group. However, glucose, TC and TG levels in serum were significantly decreased in LRC-administrated groups compared with STZ-control group. In histopathological analysis of kidney, liver and lung, both LRC- and CF-administrated groups showed the inhibition of morphological damage. Conclusions : These results suggest that LRC and CF have a biological action on STZ-induced diabetes in rats via decreasing the serum TG and TG levels and may protect the morphological changes of kidney, liver and lung.
Choi, Na Ri;Jo, Sung Hyeon;Lee, Se-Eun;Lee, Min Ji;Cho, Suin
The Korea Journal of Herbology
/
v.35
no.1
/
pp.1-8
/
2020
Objectives : This study was conducted to evaluate the effects of Corni Fructus, the dried fruits of Cornus officinalis Sieb., on unilateral common carotid artery occlusion (UCCAO) in mouse model. Methods : The Corni Fructus used in the experiment was extracted with anhydrous methanol, then filtered and freeze-dried. C57BL/6 mice used in the experiments were conducted left UCCAO surgery to set up UCCAO rodent model for mice. The mice were divided into five groups for evaluate the effect of methanol extract of Corni Fructus (COM) on UCCAO induced ischemic brain injury. The expression levels of nitric oxide in cerebrum and serum, body weight change were measured. To determine the effect of UCCAO and COM administration on brain neurons, morphological changes of the cerebrum through a microscope was conducted. And western blot was performed to confirm the underlying mechanism of neuroprotective effect of COM administration. Results : COM administered UCCAO groups (CO50, CO150, and CO500) had no significant effects on nitric oxide production in ipsilateral hemisphere proteins and sera. The CO500, 500 mg/kg COM administration, attenuated UCCAO-induced p38 inflammatory signaling pathway and inflammatory mediators such as iNOS and COX-2. The CO500 group showed resilient morphological changes of hippocampus neuronal cells about brain damage caused by decreased flow of blood. These group also showed decreased inflammation and cellular stress response in neuronal cells. Conclusions : From these results, COM has a neuroprotective property via moderating inflammatory factors and cellular stress inducing factors in brain cells.
PURPOSE. This study was conducted to evaluate the effects of plasma treatment of sandblasted and acid-etched (SLA) titanium implants on surface cleansing and osseointegration in a beagle model. MATERIALS AND METHODS. For morphological analysis and XPS analysis, scanning electron microscope and x-ray photoelectron spectroscopy were used to analyze the surface topography and chemical compositions of implant before and after plasma treatment. For this animal experiment, twelve SLA titanium implants were divided into two groups: a control group (untreated implants) and a plasma group (implants treated with plasma). Each group was randomly located in the mandibular bone of the beagle dog (n = 6). After 8 weeks, the beagle dogs were sacrificed, and volumetric analysis and histometric analysis were performed within the region of interest. RESULTS. In morphological analysis, plasma treatment did not alter the implant surface topography or cause any physical damage. In XPS analysis, the atomic percentage of carbon at the inspection point before the plasma treatment was 34.09%. After the plasma treatment, it was reduced to 18.74%, indicating a 45% reduction in carbon. In volumetric analysis and histometric analysis, the plasma group exhibited relatively higher mean values for new bone volume (NBV), bone to implant contact (BIC), and inter-thread bone density (ITBD) compared to the control group. However, there was no significant difference between the two groups (P > .05). CONCLUSION. Within the limits of this study, plasma treatment effectively eliminated hydrocarbons without changing the implant surface.
As the importance of the beauty to pursue beauty comes to the fore, the market size of hairdressing industry including hair dyeing is getting bigger. In case of continuously applying an oxidative dyeing agent commonly used in hair salons, as hair damage is inevitable, we investigated morphological changes of hair treated with a neutral oxidative dyeing agent. In the experiment results, Between the control and the 6N-7N experimental groups, there was a significant difference in Max. modulus and Tangential modulus according to Max. load, Max. stress, Max. elongation, Break load, Break stress, Break elongation, and strain section. There were the highest values in Max. load, Max. stress, Max. elongation, Break load, Break stress and Break elongation in the control group, and there was no tendency to decrease significantly according to the treatment of the experimental group. Max. modulus and Tangential modulus according to the strain evaluation section did not show a tendency to increase or decrease constantly, although there was a difference between the control and experimental groups. This study attempts to provide basic data for the development of oxidative dyeing agent that minimizes hair damage and to establish the foundation for understanding the correlation between hair designers' oxidative dyeing agent and hair health.
Liver tissue damage by a radiation exposure caused a jaundice and ascitic fluid e form harden atrophy. The reason for this lies in morphological damage of a liver cells. This study tried that observe damage mechanism of the cell organelles. It was especially observed mitochondria, endoplasmic reticulum and nuclear membrane associated with energy metabolizable. also, This study had with a radio-protector development research at the same time. Radio-protector was used to alliin that has an blood flow increase. Cell observation make used of transmission electron microscope(TEM). The result of an experiment, 7Gy of whole body irradiation was caused an inflammation in cell organelles and hypertrophy of the nucleus membrane. After 20 days, The hepatocyte has been observed in a damaged membrane on peroxisome, mitochondria and vacuole of the cell organelles. After 30 days, The hepatocyte has been observed in disconnected ribosomes on a rough endoplasmic reticulum. There was looked a giant lipoblast. There was clearly normal observed a mitochondria and nucleus membrane in the hepatocyte after alliin injection. aslo, It was no damaged the nucleus membrane. therefore, It was identified portion a radio-protector effect from alliin.
In order to investigate a pathogenesis of liver damage induced by skin burn, thermal injury was induced by scald burn on entirely dorsal surface in rats (total burn surface area $20\sim25\%$) except for inhalated injury. At 5 and 24 h after scald burn, biochemical assay and morphological changes in serum and liver tissue were examined. Skin burn increased liver weight (% of body weight, p<0.05) and the activity of serum aniline amino-transferase (ALT, p<0.05), in addition, the activity of xanthine oxidase (XO), an enzyme of oxygen free radical generating system, was elevated (p<0.01) in serum, but not in skin and in liver. Postburn treatment of allopurinol intraperitoneally decreased liver weight, serum ALT activity and serum XO activity. Scald burn induced ultrastructurally swelling of endoplasmic reticulum, ribosome detachment, accumulation of lipid, dilatation of bile canaliculi and intercellular space, neutrophil infiltration, activation of Kupffer's cells and degeneration of hepatocytic microvilli. Futhermore , thermal injury decreased not only the protein concentration in plasma but also the number of intravascular leukocytes, that indicates induction of edema formation with protein exudation and inflammation by neutrophil infiltration into the internal organs. However allopurinol injection after burn inhibited post burn ultrastructural changes. These data suggest that acute dermal scald burn injury leads to liver damage, that is related to elevation of xanthine oxidase activity in serum. Xanthine oxidase may be a key role in the pathogenesis of liver damage induced by skin burn.
Korean Journal of Agricultural and Forest Meteorology
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v.14
no.4
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pp.246-253
/
2012
Despite frequent freezing injury to tea trees due low temperature, drought, and strong wind during wintertime, no comprehensive measurements have been taken. We selected and examined 9 locations in Hwagae-myeon and 4 places in Agyang-myeon, Hadong-gun, Gyeonsanggnam-do where low temperature damage had occurred between December 2010 and February 2011. Our objective is to examine the effect of frost damage on the morphological symptom and harvest of a tea tree exposed to a constant low temperature environment during wintertime. The results of our analyses on meteorological environment, tea leaf chromaticity, water content and trypan blue are as follows: (1) the number of days with temperature of $-10^{\circ}C$ or less, which were subject to frost damage to a tea tree were 8 and 13.6% during the winterization period in 2011; (2) the accumulated time was 1,308 minutes, and the longest duration at $-10^{\circ}C$ was 588 minutes from 21:08 p.m. 15 January to 7:30 a.m. $16^{th}$ January. The rainfall was only 104 mm which was 306 mm less than the previous year; (3) the lightness L values in 2011 were higher than in 2012 due to dehydration and necrosis by blue discoloration and red discoloration at all areas in chromaticity measurement; (4) the water content in a tea leaf in 2011 was higher than in 2012 due to low rainfall and strong wind, and almost no cell death phenomenon was observed from normal tea leaves subject to no low temperature stress in a trypan blue analysis; and (5) partial coloration due to cell death, however, took place in the leaves damaged by blue discoloration subject to low temperature stress, and most coloration due to cell death took place in the leaves damaged by red discoloration.
Objectives : This study was carried out to determine whether Juglandis Semen herbal acupuncture (JSA) exerts the protective effect against toxic agent-induced live. cell damage. Methods : The cell damage was estimated by measuring lactate dehydrogenase (LDH) release, and lipid peroxidation was estimated by measuring maiondialdehyde (MDA), a product of lipid peroxidation, in rabbit liver slices. Results : When tissues were incubated with 0.5 mM Hg for $10{\sim}120\;min$, LDH release and lipid peroxidation were increased as a function of incubation time, and these effects were significantly prevented by addition of 0.1% JSA. Hg increased LDH release and lipid peroxidation in dose-dependent manner over the range of $0.1{\sim}l\;mM$ concentrations, which were reduced by 0.1% JSA. When tissues were treated with 0.5 mM Hg in the presence of $0.05{\sim}l\;%$ JSA, LDH release and lipid peroxidation induced by Hg were prevented by JSA in a dose-dependent fashion. JSA at 0.5 and 1% prevented completely effects of 0.5 mM Hg. When tissues were treated with 0.5 mM Hg for 60 min, LDH release and lipid peroxidation were increased, which were significantly prevented by addition of 0.1 % JSA. tert-Butyl hydroperoxide (tBHP) increased LDH release and lipid peroxidation, which were significantly reduced by 0.1 % JSA. Such protective effects were similar to those of N,N'-diphenyl-p-phenylenediamine (DPPD), a potent antioxidant. When tissues were treated with 0.5 mM Hg, activities of catalase and glutathione peroxidase were inhibited, and glutathione content was also reduced. Such effects were prevented by JSA, but not by DPPD. JSA prevented Hg-induced morphological changes. Conclusions : These results indicate that JSA exerts the protective effect against liver cell injury induced by toxic agents through antioxidant action, and this effect may be attributed to an increase in activities of endogeous anitoxidant enzymes and GSH content. However, antioxidant effect of JSA is different from that of a well-known potent antioxidant DPPD.
High voltage pulsed electric fields (PEF) treatment is one of the more promising nonthermal technologies to fully or partially replace thermal processing. The objective of this research was to investigate the microbial inactivation mechanisms of PEF treatment in terms of intra- and extracellular changes in the cells. Saccharomyces cerevisae cells treated with PEF showed cellular membrane damage. This resulted in the leakage of UV-absorbing materials and intracelluar ions, which increased with increasing treatment time and electric fields strength. This indicates that PEF treatment causes cell death via membrane damage and physical rupture of cell walls. We further confirmed this by Phloxine B staining, a dye that accumulates in dead cells. Using scanning and transmission electron microscopy, we observed morphological changes as well as disrupted cytoplasmic membranes in PEF treated S. cerevisae cells. In addition, PEF treatment led to damaged chromosomal DNA in S. cerevisiae.
Journal of Physiology & Pathology in Korean Medicine
/
v.22
no.6
/
pp.1462-1469
/
2008
The purpose of the study was to confirm what effect HRHDT treatment had on cell extinction by damage of endoplasmic reticulum induced to PC-12 cell damage by glucose deprivation. The study confirmed what effect it had on forming the condition of glucose deprivation within a culture fluid of PC-12 cell and on a nerve cell's survival rates and tested whether HRHDT could prevent extinction of PC-12 cell by glucose deprivation. Also, the study confirmed what effect HRHDT treatment had on the emitted quantity of LDH by glucose deprivation. To examine PC-12 cell's behavioral change under the condition of glucose deprivation and a protective effect of HRHDT on the change, the study observed PC-12 cell's behavioral change with a microscope. Also, the study confirmed density of calcium ion within cells followed by a culture time in the condition of glucose deprivation with FACS and confirmed what effect HRHDT treatment had on the above density of calcium ion within cells. Finally, the study carried out the western blot and confirmed what effect HRHDT treatment had on revelation of GRP 78 and CHOP protein and a segmental type of aspase 12. In this study, HRHDT rescued PC-12 cells from glucose deprivation-induced cell death. HRHDT also prevents the LDH release, Ca++ accumulation, and morphological change, which was associated with the ER stress. Furthermore, HRHDT reduced the expression of ER chaperone (Grp78 and CHOP) proteins by glucose deprivation in PC-12 cells. These results suggest that HRHDT might provide a useful therapeutic strategy in treatment of the neurodegenerative diseases caused by glucose deprivation injuries.
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