Cisplatin is one of the most potent chemotherapy agents. However, its use is limited due to its toxicity in normal tissues, including the kidney and ear. In particular, nephrotoxicity induced by cisplatin is closely associated with oxidative stress and inflammation. Heme oxygenase-1(HO-1), the rate-limiting enzyme in the heme metabolism, has been implicated in a various cellular processes, such as inflammatory injury and anti-oxidant/oxidant homeostasis. Capsaicin is reported to have therapeutic potential in cisplatin-induced renal failures. However, the mechanisms underlying its protective effects on cisplatin-induced nephrotoxicity remain largely unknown. Herein, we demonstrated that administration of capsaicin ameliorates cisplatin-induced renal dysfunction by assessing the levels of serum creatinine and blood urea nitrogen (BUN) as well as tissue histology. In addition, capsaicin treatment attenuates the expression of inflammatory mediators and oxidative stress markers for renal damage. We also found that capsaicin induces HO-1 expression in kidney tissues and HK-2 cells. Notably, the protective effects of capsaicin were completely abrogated by treatment with either the HO inhibitor ZnPP IX or HO-1 knockdown in HK-2 cells. These results suggest that capsaicin has protective effects against cisplatin-induced renal dysfunction through induction of HO-1 as well as inhibition oxidative stress and inflammation.
NUCB2/nesfatin-1 is first known to be expressed in the hypothalamus while controlling appetite and energy metabolism. However, recent studies have shown that NUCB2/nesfatin-1 was expressed in the various organs as well as the hypothalamus. Our previous reports also demonstrated that NUCB2/nesfatin-1 was expressed in the ovary, testis, pituitary gland, lung, kidney, and stomach of fetal and adult mice. However, the role of NUCB2/nesfatin-1 in mouse fetus remains unknown. Thus, the aim of this study was to investigate whether NUCB2/nestatin-1 is expressed in mouse fetus at the developmental stage in which organogenesis begins. To do this, we performed in situ hybridization (ISH) and immunohistochemistry (IHC) staining to examine the distribution of NUCB2 mRNA and nesfatin-1 protein in the mouse fetal organs during early developmental stages, especially at embryonic day (E) 10.5. As a result of ISH, NUCB2 mRNA positive signals were more frequent in the liver, but there were relatively few positive signals in heart. On the other hand, no positive signals were detected in other organs. These ISH results were validated by IHC staining and qRT-PCR analysis. Expression of nesfatin-1 protein detected by IHC staining was similar to that of NUCB2 mRNA detected by ISH in the liver and heart. In addition, the levels of NUCB2 mRNA expression analyzed by qRT-PCR were significantly increased in the liver and heart compared to other organs of the mouse fetus at E13.5, whereas its level was extensively decreased in the liver, but increased in the lung, stomach, and kidney of the mouse fetus at E17.5. These results suggest that NUCB2/nesfatin-1 may play an important role in liver and heart development and physiological functions in the developmental process of mouse fetus. Further studies are needed on the function of NUCB2/nesfatin-1, which is highly expressed in the various organs, including liver and heart during mouse development.
Jeong, Jin Young;Kim, Byeonghyeon;Ji, Sang Yun;Baek, Youl Chang;Kim, Minji;Park, Seol Hwa;Kim, Ki Hyun;Oh, Sang-Ik;Kim, Eunju;Jung, Hyunjung
Food Science of Animal Resources
/
v.41
no.6
/
pp.1022-1035
/
2021
This study estimated the effect of exposure to propiconazole through implementation and residues in finishing pigs. We analyzed the expression of fibrosis-related genes and performed histological analysis of the blood, liver, kidney, muscle, ileum, and fat tissues. The animals were exposed for 28 d to different concentrations of propiconazole (0.09, 0.44, 0.88, 4.41, and 8.82 mg/kg bw/d). Quantitative, gene expression, and histological analyses in tissues were performed using liquid chromatography mass spectrometry, real-time PCR, and Masson's trichrome staining, respectively. Final body weight did not differ among groups. However, genes involved in fibrosis were significantly differentially regulated in response to propiconazole concentrations. Glucose, alanine aminotransferase, and total bilirubin levels were significantly increased compared with those in the control group, while alkaline phosphatase level was decreased (p<0.05) after exposure to propiconazole. The residue limits of propiconazole were increased in the finishing phase at 4.41 and 8.82 mg/kg bw/d. The liver, kidney, and ileum showed blue staining after propiconazole treatment, confirmed by Masson's trichrome staining. In conclusion, these findings suggest that propiconazole exposure disturbs the expression of fibrosis-related genes. This study on dietary propiconazole in pigs can provide a basis for determining maximum residue limits and a better understanding of metabolism in pigs and meat products.
BACKGROUND/OBJECTIVES: Patients with chronic kidney disease (CKD) have a high concentration of uremic toxins in their blood and often experience muscle atrophy. Indoxyl sulfate (IS) is a uremic toxin produced by tryptophan metabolism. Although an elevated IS level may induce muscle dysfunction, the effect of IS on physiological concentration has not been elucidated. Additionally, the effects of ursolic acid (UA) on muscle hypertrophy have been reported in healthy models; however, it is unclear whether UA ameliorates muscle dysfunction associated with chronic diseases, such as CKD. Thus, this study aimed to investigate whether UA can improve the IS-induced impairment of mitochondrial biogenesis. MATERIALS/METHODS: C2C12 cells were incubated with or without IS (0.1 mM) and UA (1 or 2 μM) to elucidate the physiological effect of UA on CKD-related mitochondrial dysfunction and its related mechanisms using real-time reverse transcription-polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay. RESULTS: IS suppressed the expression of differentiation marker genes without decreasing cell viability. IS decreased the mitochondrial DNA copy number and ATP levels by downregulating the genes pertaining to mitochondrial biogenesis (Ppargc1a, Nrf1, Tfam, Sirt1, and Mef2c), fusion (Mfn1 and Mfn2), oxidative phosphorylation (Cycs and Atp5b), and fatty acid oxidation (Pdk4, Acadm, Cpt1b, and Cd36). Furthermore, IS increased the intracellular mRNA and secretory protein levels of interleukin (IL)-6. Finally, UA ameliorated the IS-induced impairment in C2C12 cells. CONCLUSIONS: Our results indicated that UA improves the IS-induced impairment of mitochondrial biogenesis by affecting differentiation, ATP levels, and IL-6 secretion in C2C12 cells. Therefore, UA could be a novel therapeutic agent for CKD-induced muscle dysfunction.
For the purpose of making clear the activity of the alkaline phosphatase to the morphogenesis and function of the various structures of the developing chick kidney in relation to PAS-positive materials and phospholipid, the author observed histochemically the aforementioned enzyme and other substances. The mesonephros and metanephros of 4-20 day white leghorn embryos were used, obtaining the following results. 1. Before definite appearance of the secretory tubules the alkaline phosphatase activity showed strongly in the undifferentiated mesenchymal tissue. As the tubules grew differentiated, the alkaline phosphatase activity was found to have disappeared in the mesenchymal tissue surrounding the tubules. The above mentioned fact indicates that the alkaline phosphatase may be concerned with morphogenesis of the developing chick kindney. 2. The fact that the strong alkaline phosphatase activity and the occurrence of the PAS-positive materials were observed at the luminal borders of differentiated secretory tubules of mesonephros and metanephros, indicates that alkaline phosphatase may be concerned with reabsorption of carbohydrate at the borders. 3. A strong positive reaction of phospholipid was found in the cytoplasm and brush borders of the mesonephric and metanephric tubules. The fact that vicissitude of alkaline phosphatase was found to coincide with that of phospholipid suggests that the enzyme may have influence on the metabolism of the phospholipid.
The effects of age and dietary fatty acid composition on lipid metabolism were investigated in Sprague-Dawley strain male rats. These animals weighing 88.6$\pm$2.2g were fed 10% dietary fat(W/W, 20% of total energy) with 0.5, 1, 2 P/S ratio and in each P/S ratio there were three different levels of n-6/n-3 fatty acid ratio ; 2, 4, 8. The experimental period was 1 month, 6 months and 12 months. The results of this study were as follows. The body weight of rats increased rapidly for the first two months, then increased slowly until 7 to 8 months. After 10 months of dietary regimen their weight decreased. The weight of liver, kidney and epidydimal fat pad increased along with the body weight and then decreased in the 12 months. Plasma total lipid increased with age and it decreased significantly when P/S ratio of dietary fatty acid was high. In creased with age and it decreased significantly when P/S ratio of dietary fatty acid was high. In creasing n-3 fatty acid intake in each P/S ratio resulted in lower plasma total lipid although was not statistically significant. The amount of plasma total cholesterol increased at 6 months, but decreased at 12 months. In case of 1, 12 months, increasing P/S ratio significantly plasma total cholesterol and LDL-cholesterol were decreased and hepatic cholesterol was increased, VLDL-HDL-cholesterol did not changed. The n-6/n-3 ratio did not affect any of theses. The amount of plasma triglyceride and VLDL-triglyceride increased at 6 month then decreased. When the rats consumed higher amount of n-3 fatty acid in each P/S ratio, their plasma triglyceride and hepatic triglyceride increased at 1, 12months.
This study investigated the effect of enteral nutrition supplementation on glucose and lipid metabolism in non-insulin dependent diabetes mellitus(NIDDM) patients(n=29). Nutrition formula(400kcal/day) were supplied daily for eight weeks as a substitute for a snack or a meal. Subjects were divided into three groups based on changes of fasting blood glucose(FBG), glucose response area(GRA) on oral glucose tolerance test(OGTT), before and after intake of nutrition formula : group 1(the group of a decrease in FBG and GRA, n=20), group 2(the group of a decrease in FBG and an increase in GRA, n=4), and group 3(the group of an increase in FBF and GRA, n=5). Before nutrition supplementation, group 3 showed a longer tendency of DM duration and a lower tendency of insulin and C-peptide response are than those of group 1 and 2. At 8 weeks after nutrition supplementation, group 1 showed a significant increase in insulin and C-peptide response areas but group 2 and 3 showed no change in those areas. After nutrition supplementation, all three groups showed a tendency of decrease in glycated hemoglobin and no significant changes in the levels of serum triglycerides, HDL, LDL, total cholesterol, albumin, transferrin, creatinine, GOT and GPT. The results suggest that using an enteral nutrition formula in NIDDM patients is a good substitute for a meal or snack and could improve blood glucose control without any changes in lipid levels, and liver and kidney functions. The beneficial effect of nutrition supplementation on glycemic control resulted from components of nutrition formula had such as additional fiber and high monounsaturated fatty acid as the source of fat to be helpful 세 glycemic control in diabetics.
This experiment was designed to investigate the effects of the mixing ratio of soyprotein and casein, and the level of pectin combined with the mixture on lipid metabolism in rats. Forty-eight male weanling rats of Wistar strain weighing 58.8\;{\pm}\;1.9g$ were divided into six groups by completely randomized block design and fed 10% protein diet for four weeks. Two types of protein mixtures (casein to soyprotein mixing ratio of 1 : 3 and 2: 1)combined with 0.5% , 3%, and 5% of pectin were employed for experimental diets. The results obtained in the study are summarized as follows ; 1) Feed efficiency ratio and protein efficiency ratio were not significantly different among six groups for the whole experimental period, but those for high casein-low pectin group were significantly higher than the ones for high soy-high pectin group at 4th week of the experimental period. 2) Gross fecal dried weight and fecal lipid excretion were higher in high pectin groups of both protein combinations. Therefore, the apparent fat digestibility and absorption appeared to be significantly low in high pectin groups. 3) Pectin was effective in lowering serum lipid and cholesterol levels in high casein groups, but no effect of pectin was noted in high soyprotein groups. 4) Lipid and cholesterol contents of the liver were higher in high soy-low pectin group than the others. And no marked differences in lipid and cholesterol contents in the kidney and carcass were observed.
Cancer, a serious public health problem in worldwide, results from an excessive and uncontrolled proliferation of the body cells without obvious physiological demands of organs. The gastrointestinal tract, including the esophagus, stomach and intestine, is a unique organ system. It has the highest cancer incidence and cancer-related mortality in the body and is influenceed by both genetic and environmental factors. Among the various chemical elements recognized in the nature, some of them including zinc, iron, cobalt, and copper have essential roles in the various biochemical and physiological processes, but only at low levels and others such as cadmium, lead, mercury, arsenic, and nickel are considered as threats for human health especially with chronic exposure at high levels. Cadmium, an environment contaminant, cannot be destroyed in nature. Through impairment of vitamin D metabolism in the kidney it causes nephrotoxicity and subsequently bone metabolism impairment and fragility. The major mechanisms involved in cadmium carcinogenesis could be related to the suppression of gene expression, inhibition of DNA damage repair, inhibition of apoptosis, and induction of oxidative stress. In addition, cadmium may act through aberrant DNA methylation. Cadmium affects multiple cellular processes, including signal transduction pathways, cell proliferation, differentiation, and apoptosis. Down-regulation of methyltransferases enzymes and reduction of DNA methylation have been stated as epigenetic effects of cadmium. Furthermore, increasing intracellular free calcium ion levels induces neuronal apoptosis in addition to other deleterious influence on the stability of the genome.
Using the $Methionine-2-C^{14}$, the metabolism of methionine to the experimental rats on rice diet was studied comparing with that to the rats on stock diet in this paper. The National Institute of Health strain of weaning albino rats were housed into the individual cages deviding into 2 groups, the rice diet (RD) group and the stock diet (SD) group, and fed on rice diet and stock diet respectively for 10 weeks. On the day of experiment, the rats were parenterally administered. the $methionine-2-C^{14}$ solution after fasting over night. And then the rats were sacrificed by ether anesthesia by time being of one, three, six, and twelve hours each and the organs, pituitary gland, pancreas, spleen, liver, and kidney, were taken out for the determinations of radioactivities. And also the excretion of radioactivities through urine were determined by time being. The radioactivities were determined by Autoscaler SC-51 using the planchets. The results of radioactivities of urine excretion were shown at table 3 and the results of radioactivities distibutions in the organs by time being after parenteral administration of $methionine-2-C^{14}$ were shown table 4 in the original paper. According to the results, the following are summarized; 1. The growth experiment result of rats on. rice diet and stock diet were same as shown by the previous workers indicating significant growth inhibition at the rice diet group. 2. Due to the result of radioactivity excretion through urine after administration of $methionine-2-C^{14}$, it might he considered that methionine in the rice diet seems to be limited. However, it seems to be not 주 mostly limited. 3. And due to the results of radioactivity distribution in the organs by time being, the radioactivity in the liver tissue showed appearently higher readings at this methionine study compared with the results at the lysine study shown by HAW and his co-worker. This might be interpreted, though it is not clear, that liver might require methionine as a deficient amino acid at the tissue because methionine is limited at the rice diet.
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