• Journal of Life Science
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• v.19 no.10
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• pp.1417-1423
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• 2009

Previous studies have suggested that docosahexaenoic acid (DHA) supplementation into n-3 fatty acid deficient diet improved spatial learning performance, but there was no significant difference in brain related function when DHA was added into a n-3 fatty acid adequate diet. Here, we investigated the effect of adding DHA into an n-3 fatty acid deficient or adequate diet on brain and liver fatty acid composition. On the second day after conception, Sprague Dawley strain dams were divided into four groups as follows; n-3 fatty acid deficient (Def), n-3 fatty acid deficient plus DHA (Def+DHA, 10.2% DHA), n-3 fatty acid adequate (Adq, 3.4% linolenic acid), and n-3 fatty acid adequate plus DHA (Adq+DHA, 3.31% linolenic acid plus 9.65% DHA). After weaning, male pups were fed on the same diets of their respective dams until adulthood. In brain fatty acid composition, the Def group showed a lower brain DHA (64% decrease), which was largely compensated for by an increase in docosapentaenoic acid (22:5n-6). Brain DHA in the Def+DHA group was increased to almost the same extent as in the Adq and Adq+DHA groups and there were no significant differences among them. Liver fatty acid composition showed a similar pattern to that of the brain, but liver DHA in the Def+DHA showed the highest percentage among the diet groups. In conclusion, n-3 fatty acid deficiency from gestation to adulthood leads to decreased brain DHA, which has been shown to be highly associated with poor spatial leaning performance. Thus, adequate brain DHA levels are required for optimal nervous function.

• The Korean Journal of Food And Nutrition
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• v.29 no.4
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• pp.521-528
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• 2016

This study was conducted to investigate changes in the proximate composition, antioxidant activities, and ${\alpha}$-glucosidase inhibitory activity of Opuntia ficus-indica (OFI) cladodes cultivated in Jeju (JJ1, JJ2, JJ3) and Jeonnam (JN1, JN2). The difference in the proximate composition (crude protein, lipid and ash content) of OFI between the two regions was not significant. Ca, Mg and Na were the major mineral components of OFI. The ascorbic acid content of OFI ranged from 57.87 to 143.72 mg/100 g. A 70% ethanol extract was used to investigate the antioxidant content and activity as well as the ${\alpha}$-glucosidase inhibitory activity. The total polyphenol and flavonoid contents of OFI were 38.69~55.29 and 3.33~4.03 mg/g, respectively. The antioxidant activities based on the DPPH and ABTS free radical scavenging assays were 45.19~61.52% and 39.15~51.96%, respectively, at a concentration of 1 mg/mL. The inhibitory activity of OFI extracts against rat intestinal ${\alpha}$-glucosidase was 29.72~45.73% at 1 mg/mL concentration, and JN1 showed the highest ${\alpha}$-glucosidase inhibitory activity. This information could be very useful for authentication of Opuntia species with the highest potential as sources of nutritional and therapeutic elements.

• The Korean Journal of Food And Nutrition
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• v.22 no.1
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• pp.48-56
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• 2009

This study was conducted to examine the effects of Opuntia ficus-indica complexes(OCB) on the intake of water and food, body weight, blood glucose levels, glucose tolerance and lipid metabolism in streptozotocin(STZ)-induced diabetic rats. Thirty-two male Sprague-Dawley rats were assigned to four different groups; non-diabetic control(NC), diabetic control (DC), diabetic OCB of 2%(OCB-2), and diabetic OCB of 5%(OCB-5). The animals were fed on each experimental diet for 3 weeks. The DC, OCB-2 and OCB-5 groups showed a higher intake of water and food than the NC group. The fasting blood glucose levels were 100 $ mg/d{\ell}$ and 416 $ mg/d{\ell}$ for the NC and DC groups, respectively. The OCB-5 group presented a significantly low fasting glucose level of 21%(P<0.05), while OCB-2 group had a decrease of 13% compared to the DC group. As for the results of the glucose tolerance test, the highest blood glucose level was observed for all the groups at 30 minutes after the glucose injections as well as higher plasma insulin levels in the OCB-5 group. Plasma total cholesterol, triglyceride, non-esterified fatty acids(NEFA) and LDL-cholesterol concentrations were also lower in the OCB-2 and OCB-5 groups. The experimental diet did not affect the HDL-cholesterol levels. The overall results suggest that the higher intake of food by the OCB-2 and OCB-5 groups improved the blood glucose levels and lipid metabolism in STZ-induced diabetic rats.

• Journal of Yeungnam Medical Science
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• v.10 no.2
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• pp.313-337
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• 1993

The aim of this study was to clarify the role of Kupffer cells in the mechanism of endotoxin-induced liver injury. The study on fine structure of Kupffer cells was performed after the injection of endotoxin. The endotoxin(Escherichia coli lipopolysaccharide 026 : B6. 1.5mg/100 g of body weight) was intraperitoneally injected in Sprague-Dewley rats. Animals were sacrificed at 1/4, 1/2, 1, 2, 4, 8, 16, 24, 72 and 120 hours after the injection of endotoxin. Livers were extirpated and processed to be examined by light and electron microscopy. The results obtained were summerized as follows: Early changes observed in liver after endotoxin injection included the increased number and hypertrophy of Kupffer cells, infiltration of neutrophils and presence of fibrin thrombi within the sinusoids. The continuous increase of the Kupffer cells in number with hypertrophy, congestion and infiltration of inflammatory cells within the sinusoids were observed. Hepatocytes showed fatty change and occasional necrosis. At 72 hours the congestion decreased. At 120 hours the number of Kupffer cells was increased, but the morphology of Kupffer cells became similar to that of the control group. The numbers and sizes of primary and secondary lysosomes and amount of euchromatin of Kupffer cells increased. Swellings and increase in number of mitochondria, Golgi complex, smooth endoplasmic reticulum, rough endoplasmic reticulum were evident. Microthrombi were present within the sinusoids. The swelling of rough endoplasmic reticulum and mitochondria, decrease of glycogen particles, fatty change, hypoxic vacuoles, pyknotic nuclei and occasional necrosis were observed in hepatocytes. At 72 hours the number of secondary lysosomes in Kupffer cells decreased. At 120 hours the morphology of Kupffer cells became similar to that of the control group. According to these results, it was postulated that the endotoxin was initially taken up by pinocytosis into Kupffer cells and degraded in secondary lysosomes of activated Kupffer cells. Kupffer cells may play an important role in the defense mechanism of liver during endotoxemia. The dysfunction of Kupffer cells and ischemia by sinusoidal microthrombi may cause liver injury.

• Journal of dental hygiene science
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• v.15 no.4
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• pp.424-429
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• 2015

The aim of this study was to investigate whether peripheral or central administration of triptolide is involved in pain modulation in inflammatory orofacial pain. The inflammatory orofacial pain was induced by the injection of 5% formalin into right vibrissa pad of rats. The pain behavioral response was measured the number of grooming or scratching on the orofacial area for 9 successive 5 minutes intervals. Triptolide was administrated into the identified vibrissa pad (12.5, 25, $50{\mu}g/50{\mu}l$) or intracisternal space (0.01, 0.1, $1{\mu}g/10{\mu}l$) 10 min before formalin injection. The nociceptive responses were reduced in the 2nd phase (11~45 minutes), particularly 20, 30 minutes after fomalin injection following administration of triptolide into vibrissa pad (25, $50{\mu}g/50{\mu}l$). Intracisternal ($1{\mu}g/10{\mu}l$) administration of triptolide alleviated the formalin-induced pain behaviors in the 2nd phase, especially 25~40 minutes after formalin injection. Triptolide could be a promising analgesic agent in the treatment of inflammatory orofacial pain.

• Development and Reproduction
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• v.10 no.2
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• pp.147-154
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• 2006

Phthalates such as di(2-ethyl hexyl)phthalate(DEHP) are industrial chemicals with wide-ranging human exposures because of their use in plastics and other common consumer products. Consequently, their adverse effects as endocrine disruptor in the reproductive physiology of both laboratory rodents and human have been studied extensively. The present study was undertaken to examine whether prepubertal exposure to DEHP affects on the onset of puberty and the associated reproductive parameters such as hormone receptor expressions in female rats. DEHP(100mg/kg/day) was administered daily from postnatal day 25(PND 25) through the day when the first vaginal opening(VO) was observed, and the animals were sacrificed on the next day. Gross anatomy and weight of reproductive tissues were compared to test the DEHP's effects on the cell proliferation. Furthermore, histological studies were performed to assess the structural alterations in the tissues. Specific radioimmunoassay was carried out to measure serum LH levels. To determine the transcriptional changes in progesterone receptor(PR), total RNAs were extracted and applied to the semi-quantitative reverse transcription polymerase chain reaction(RT-PCR). As a result, delayed VO was shown in the DEHP group(PND $37.3{\pm}0.7$) compared to the control group(PND $35.3{\pm}0.7$; p<0.05). DEHP treatment significantly decreased the wet weight of ovaries and uteri compared to the control group(p<0.05). Interestingly, elevation of serum LH levels was shown in the DEHP group(p<0.05). Graafian follicles and corpora lutea were observed only in the ovaries from the control animals. Numerous primary, secondary follicles and small atretic follicles were observed in the ovaries from DEHP-treated animals. Similarly, hypotrophy of luminal and glandular uterine epithelium was found in the DEHP-treated group. These effects were probably due to the inhibitory effects of DEHP on the synthesis and secretion of estrogen from granulosa cells. In the semiquantitative RT-PCR studies, the transcriptional activities of PR in both ovary(p<0.05) and uterus(p<0.01) from DEHP-treated animals were significantly lower than those from the control animals. The present studies demonstrated that the acute exposure to DEHP during the critical period of prepubertal stage could inactivate the reproductive system resulting delayed puberty in female rats.

• Applied Microscopy
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• v.38 no.3
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• pp.151-157
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• 2008

Trigeminal primary afferents expressing $P2X_3$ or transient receptor potential vanilloid 1 (TRPV1) are involved in the transmission of nociceptive information. In order to characterize $P2X_3$- and TRPV1-immunopositive neurons in the trigeminal ganglion (TG) and trigeminal caudal nucleus (Vc), we performed immunofluorescence experiments using anti-$P2X_3$ and anti-TRPV1 antisera and a morphometric analysis. 77.4% (1,401/1.801) of all the $P2X_3$-postive neurons coexpressed TRPV1 and 51.9% (1,401/2,698) of all the THFV1-immunopositive neurons also costained for $P2X_3$ in the TG. Immunoreactivity for both $P2X_3$ and TRPV1 were present in medium-sized neurons but not in small- and large-sized neurons. $P2X_3$ and/or TRPV1-immunopositive fibers were observed in the primary afferents and their associated axons in the Vc. These fibers and terminals were distributed in the superficial lamina of Vc: $P2X_3$-immunopositive fibers and terminals were distributed in the lamina I and II, expecially in the inner part of lamina II (lamina IIi), whereas TRPV1-immunopositive ones were densely detected in the lamina I and outer part of lamina II (lamina IIo). Immunopositive fibers and terminals for both $P2X_3$ and TRPV1 were observed on the border between lamina IIi and IIo. These results suggest that terminals coexpressing $P2X_3$ and TRPV1 are involved in specific roles in the transmission and processing of orofacial nociceptive information.

• Childhood Kidney Diseases
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• v.6 no.2
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• pp.169-177
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• 2002

Purpose: Hypertension accelerates the progression of chronic renal disease, whether it results from, or causes, the renal disease. Therefore, the control of hypertension is one of the important factors that retard the rate of renal deterioration. We compared the effects of different antihypertensive agents on renal function and glomerular morphology In subtotal nephrectomized rats. Materials and methods: After induction of chronic renal failure with 5/6 nephrectomy, the rats were divided into three groups; control group (Group C), enalapril group (Group E), and nicardipine group (Group N). Systolic blood pressure was measured by tail cuff method every 4 weeks until 12 weeks after nephrectomy. At 12 weeks after nephrectomy, all rats were placed in metabolic cages for 24 hour urine collections to measure urinary protein and creatinine excretion. After urine collection and blood sampling for serum creatinine, all rats were sacrificed. The renal tissue was processed for morphometric study with light microscope and electron microscope. Results: 1. The blood pressure of Group C increased progressively, but both enalapril and nicardipine prevented the development of hypertension, and the two drugs were equally effective in maintaining normal blood pressure throughout the study. 2. Twenty-four hour urinary protein excretion was lower in Group E compared to Group C and Group N 3. Mesangial expansion score in both treated groups were significantly lower than the control group. Mean glomerular volume in Group E was significantly reduced compared to Group C and Group N. There was no significant difference in mean glomerular volume between Group C and Group N. 4. There was no significant difference in podocyte structural changes, estimated by filtration slit length density, among control, enalapril and nicardipine treated groups. Conclusion: Control of hypertension with enalapril or nicardipine afforded considerable protection from mesangial expansion in the rat remnant kidney model. But protein excretion and glomerular growth were significantly reduced in Group E compared to Group N. There was no significant difference in podocyte structural changes among the 3 groups.

• Childhood Kidney Diseases
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• v.3 no.1
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• pp.35-41
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• 1999

Purpose The single administration of PAN(Puromycin-Aminonudeoside) to rats results in nephropathy that are similar to human minimal change nephrotic syndrome. Recently several studies indicate the pathophyslological importance of oxygen free radicals in rats with PAN-induced nephrosis. This study was conducted to evaluate the effect of $\alpha$-tocopherol, an oxygen free radical scavenger, on the histologic and biochemical changes of PAN-induced nephrosis in rats. Methods : Twenty-one Sprague-Dawley rats weighing 180-300 gm were divided into 3 groups. In group I (control group), the rats were given saline intraperitoneally for 12 days, in group II the rats were given PAN 7.5mg/100g of body weight intravenously one time and group III PAN intravenously, followed by $\alpha$-tocopherol 0.5 mg/100g of body weight jntramuscularly for 12 days. Twenty four hour urinary protein and creatinine excretion were measured on day 0, 5, 11 and 18. On the 18th day, rats were sacrificed for the determination of total serum protein, albumin and cholesterol levels. To estimate renal injuries by oxygen free radical, lipid peroxide concentration and reduced glutathione were measured in renal cortex. Histological examination in rat glomerular lesions were performed. Results : From the 5th days of PAN administration, urine protein/creatinine of group II and III were significantly increased compared the group I (P<0.05). But, urine protein/creatinine of group III was significantly lower than group II at 18th days (P<0.05). Total serum protein and albumin of group II were significantly lower than those of group III (P<0.05). Serum cholesterol of group II was significantly higher than that of group III (P<0.05). Lipid peroxide and reduced glutathione in renal cortex of group II were significantly higher than that of group I and III (P<0.05). Electron microscopic strudies of group II showed the loss of epithelial foot processes, but in group III showed preservation of epithelial foot processes. Conclusion : PAN-induced nephropathy was ameliorated significant recovery of foot process change and reduction of the urinary protein excretion by antioxidant, $\alpha$-tocopherol.

• Childhood Kidney Diseases
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• v.2 no.2
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• pp.138-144
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• 1998

Purpose : The use of cyclosporine and mitomycin in various immunologic or neoplastic disorders has been known to cause wide-ranged nephrotoxic effects including thrombotic microangiopathy. However, the mechanism of nephrotoxicity of these drugs has not been studied adequately, so that present experimental study has been undertaken to find out whether these drugs can cause direct damage to the kidney and to clarify the pathogenetic mechanism of nephrotoxic effect of these drugs. Materials and methods : Sprague-Dawley rats weighing 250-300 gm were used for experimental animals and unilateral renal perfusion technique, modified from the method described by Hoyer et al was used. Isolation of left kidney from systemic circulation was made by clamping aorta and left renal vein and a hole was punctured in the anterior wall of the left renal vein. Cyclosporine (2.5 mg in 4 ml solution) and mitomycin (1.6 mg in 4ml solution) were infused through left renal artery and normal saline was used in control rats. Forty-eight hours after infusion of the drugs, animals were sacrificed and left kidney removed and processed for histologic examination. Total ischemic time of left kidney was less than 15 minutes: Results : Cyclosporine-perfused group showed severe swelling of glomerular endothelial ceil along with swelling of glomerular epithelial cell and interstitial vascular endothelial cell. Mitomycin-perfused group also showed severe swelling of glomerular endothelial and epithelial cells. And in addition to these findings, they demonstrated platelets aggregation, swelling and degranulation of platelets and fibrin accumulation in some of the capillaries, indicating occurrance of thrombotic microangiopathy. Conclusion : present experiment indicates that cyclosporine and mitomycin can cause direct toxic injury to renal endothelial cell. And this direct toxic damage to endothelial cell seems to be an important initiating event for the development of thrombotic microangiopathy.