OBJECTIVE: To determine the effect of hypercholsterolemia induced by a high-lipid diet on glomerulosclerosis. METHODS: Twenty nephrotic syndrome (NS) Wistar rats administrated adriamycin (ADR) with a single intravenou...OBJECTIVE: To determine the effect of hypercholsterolemia induced by a high-lipid diet on glomerulosclerosis. METHODS: Twenty nephrotic syndrome (NS) Wistar rats administrated adriamycin (ADR) with a single intravenous dose of 5 mg/kg body weight, were divided into the standard and high-lipid chow groups. Another 20 weight-matched non-NS rats that received a vehicle alone were grouped as control. Urinary protein excretion and serum cholesterol were assayed; image analysis and techniques of pathology, immunohistochemistry, and molecular biology were used to determine morphological changes in glomeruli and the production of glomerular mesangial matrices in different groups. RESULTS: The serum total cholesterol level was significantly higher in rats with high-lipid chow in both non-NS [(2.2 +/- 0.3) g/L vs. (0.9 +/- 0.1) g/L, P展开更多
Diet-induced obesity has previously been shown to occur with the concomitant rise in the expression of proin-flammatory cytokines and increases in collagen deposition.While it has been known that the regenerative proc...Diet-induced obesity has previously been shown to occur with the concomitant rise in the expression of proin-flammatory cytokines and increases in collagen deposition.While it has been known that the regenerative process of skeletal muscle is altered in obese mice following an acute muscle injury,we sought to examine differences in the expression of various markers of extracellular matrix remodeling and repair.Our laboratory has previously reported an impaired inflammatory and protein synthetic signaling in these mice that may contribute negatively to the muscle regenerative process.To expand upon this previous investigation,tissues from these animals un-derwent further analysis to determine the extent of changes to the regenerative response within the extracellular matrix,including transcriptional changes in CollagenⅠ,CollagenⅢ,and Fibronectin.Here,we show that the expression of CollagenⅢ:Ⅰis significantly increased at 3-days post-injury in obese injured animals compared to lean injured animals(p=0.0338),and by 28-days the obese injured animals exhibit a significantly lower CollagenⅢ:Ⅰthan their lean injured counterparts(p=0.0035).We demonstrate an impaired response to an acute muscle injury in obese mice when compared with lean counterparts.However,further studies are required to elucidate translational consequences of these changes,as well as to determine any causative mechanisms that may be driving this effect.展开更多
Objective To study the antidiabetic and anti-oxidative effects of honokiol （Hon） in Magnolia officinalis and its underlying molecular mechanism in diabetic rats induced by high-fat diet （HFD） and streptozotocin （...Objective To study the antidiabetic and anti-oxidative effects of honokiol （Hon） in Magnolia officinalis and its underlying molecular mechanism in diabetic rats induced by high-fat diet （HFD） and streptozotocin （STZ）. Methods After ig administration with Hon [25, 50, and 100 mg/（kg.d）] to diabetic rats for consecutive 10 weeks, the levels of blood glucose （BG）, oral glucose tolerance （OGT）, blood lipids including total cholesterol （TC）, triglyceride （TG）, high density lipoprotein-cholesterol （HDL-C）, and low density lipoprotein-cholesterol （LDL-C）, hepatic oxidative stress including the activities of superoxide dismutase （SOD）, catalase （CAT）, glutathione peroxidase （GSH-Px）, methane dicarboxylic aldehyde （MDA）, and cytochrome P4502E1 （CYP2E1） in diabetic rats were measured. Results Compared to the diabetic control rats, ig administration of Hon resulted in significant decrease in BC, TC, TG, and LDL-C levels in serum, as well as hepatic CYP2E] activity and MDA content in diabetic rats, whereas the level of OGT and activities of hepatic CAT, SOD, and CSH-Px in diabetic rats were significantly increased. Conclusion Hon could alleviate hyperglycemia, hyperlipemia, hepatic oxidative damage, and insulin resistance in diabetic rats by inhibiting hepatic CYP2E1 activity.展开更多
Growing evidence suggests the implication of the gut microbiota in various facets of health and disease. In this review, the focus is put on microbiota-host molecular cross-talk at the gut epithelial level with specia...Growing evidence suggests the implication of the gut microbiota in various facets of health and disease. In this review, the focus is put on microbiota-host molecular cross-talk at the gut epithelial level with special emphasis on two defense systems： intestinal alkaline phosphatase（IAP） and inducible heat shock proteins（iHSPs）. Both IAP and iHSPs are induced by various microbial structural components（e.g. lipopolysaccharide, flagellin, CpG DNA motifs）,metabolites（e.g. n-butyrate） or secreted signal molecules（e.g., toxins, various peptides, polyphosphate）. IAP is produced in the small intestine and secreted into the lumen and in the interior milieu. It detoxifies microbial components by dephosphorylation and, therefore, down-regulates microbe-induced inflammation mainly by inhibiting NF-κB pro-inflammatory pathway in enterocytes. IAP gene expression and enzyme activity are influenced by the gut microbiota. Conversely, IAP controls gut microbiota composition both directly, and indirectly though the detoxification of pro-inflammatory free luminal adenosine triphosphate and inflammation inhibition. Inducible HSPs are expressed by gut epithelial cells in proportion to the microbial load along the gastro-intestinal tract. They are also induced by various microbial components, metabolites and secreted molecules. Whether iHSPs contribute to shape the gut microbiota is presently unknown. Both systems display strong anti-inflammatory and anti-oxidant properties that are protective to the gut and the host. Importantly, epithelial gene expressions and protein concentrations of IAP and iHSPs can be stimulated by probiotics, prebiotics and a large variety of dietary components, including macronutrients（protein and amino acids, especially L-glutamine, fat, fiber）, and specific minerals（e.g. calcium）and vitamins（e.g. vitamins K1 and K2）. Some food components（e.g. lectins, soybean proteins, various polyphenols） may inhibit or disturb these systems. The general cel ular and molecular mechanisms involved in the microbiota-host epithelial crosstalk and subsequent gut protection through IAP and iHSPs are reviewed along with their nutritional modulation.Special emphasis is also given to the pig, an economically important species and valuable biomedical model.展开更多
文摘OBJECTIVE: To determine the effect of hypercholsterolemia induced by a high-lipid diet on glomerulosclerosis. METHODS: Twenty nephrotic syndrome (NS) Wistar rats administrated adriamycin (ADR) with a single intravenous dose of 5 mg/kg body weight, were divided into the standard and high-lipid chow groups. Another 20 weight-matched non-NS rats that received a vehicle alone were grouped as control. Urinary protein excretion and serum cholesterol were assayed; image analysis and techniques of pathology, immunohistochemistry, and molecular biology were used to determine morphological changes in glomeruli and the production of glomerular mesangial matrices in different groups. RESULTS: The serum total cholesterol level was significantly higher in rats with high-lipid chow in both non-NS [(2.2 +/- 0.3) g/L vs. (0.9 +/- 0.1) g/L, P
文摘Diet-induced obesity has previously been shown to occur with the concomitant rise in the expression of proin-flammatory cytokines and increases in collagen deposition.While it has been known that the regenerative process of skeletal muscle is altered in obese mice following an acute muscle injury,we sought to examine differences in the expression of various markers of extracellular matrix remodeling and repair.Our laboratory has previously reported an impaired inflammatory and protein synthetic signaling in these mice that may contribute negatively to the muscle regenerative process.To expand upon this previous investigation,tissues from these animals un-derwent further analysis to determine the extent of changes to the regenerative response within the extracellular matrix,including transcriptional changes in CollagenⅠ,CollagenⅢ,and Fibronectin.Here,we show that the expression of CollagenⅢ:Ⅰis significantly increased at 3-days post-injury in obese injured animals compared to lean injured animals(p=0.0338),and by 28-days the obese injured animals exhibit a significantly lower CollagenⅢ:Ⅰthan their lean injured counterparts(p=0.0035).We demonstrate an impaired response to an acute muscle injury in obese mice when compared with lean counterparts.However,further studies are required to elucidate translational consequences of these changes,as well as to determine any causative mechanisms that may be driving this effect.
文摘Objective To study the antidiabetic and anti-oxidative effects of honokiol （Hon） in Magnolia officinalis and its underlying molecular mechanism in diabetic rats induced by high-fat diet （HFD） and streptozotocin （STZ）. Methods After ig administration with Hon [25, 50, and 100 mg/（kg.d）] to diabetic rats for consecutive 10 weeks, the levels of blood glucose （BG）, oral glucose tolerance （OGT）, blood lipids including total cholesterol （TC）, triglyceride （TG）, high density lipoprotein-cholesterol （HDL-C）, and low density lipoprotein-cholesterol （LDL-C）, hepatic oxidative stress including the activities of superoxide dismutase （SOD）, catalase （CAT）, glutathione peroxidase （GSH-Px）, methane dicarboxylic aldehyde （MDA）, and cytochrome P4502E1 （CYP2E1） in diabetic rats were measured. Results Compared to the diabetic control rats, ig administration of Hon resulted in significant decrease in BC, TC, TG, and LDL-C levels in serum, as well as hepatic CYP2E] activity and MDA content in diabetic rats, whereas the level of OGT and activities of hepatic CAT, SOD, and CSH-Px in diabetic rats were significantly increased. Conclusion Hon could alleviate hyperglycemia, hyperlipemia, hepatic oxidative damage, and insulin resistance in diabetic rats by inhibiting hepatic CYP2E1 activity.
文摘Growing evidence suggests the implication of the gut microbiota in various facets of health and disease. In this review, the focus is put on microbiota-host molecular cross-talk at the gut epithelial level with special emphasis on two defense systems： intestinal alkaline phosphatase（IAP） and inducible heat shock proteins（iHSPs）. Both IAP and iHSPs are induced by various microbial structural components（e.g. lipopolysaccharide, flagellin, CpG DNA motifs）,metabolites（e.g. n-butyrate） or secreted signal molecules（e.g., toxins, various peptides, polyphosphate）. IAP is produced in the small intestine and secreted into the lumen and in the interior milieu. It detoxifies microbial components by dephosphorylation and, therefore, down-regulates microbe-induced inflammation mainly by inhibiting NF-κB pro-inflammatory pathway in enterocytes. IAP gene expression and enzyme activity are influenced by the gut microbiota. Conversely, IAP controls gut microbiota composition both directly, and indirectly though the detoxification of pro-inflammatory free luminal adenosine triphosphate and inflammation inhibition. Inducible HSPs are expressed by gut epithelial cells in proportion to the microbial load along the gastro-intestinal tract. They are also induced by various microbial components, metabolites and secreted molecules. Whether iHSPs contribute to shape the gut microbiota is presently unknown. Both systems display strong anti-inflammatory and anti-oxidant properties that are protective to the gut and the host. Importantly, epithelial gene expressions and protein concentrations of IAP and iHSPs can be stimulated by probiotics, prebiotics and a large variety of dietary components, including macronutrients（protein and amino acids, especially L-glutamine, fat, fiber）, and specific minerals（e.g. calcium）and vitamins（e.g. vitamins K1 and K2）. Some food components（e.g. lectins, soybean proteins, various polyphenols） may inhibit or disturb these systems. The general cel ular and molecular mechanisms involved in the microbiota-host epithelial crosstalk and subsequent gut protection through IAP and iHSPs are reviewed along with their nutritional modulation.Special emphasis is also given to the pig, an economically important species and valuable biomedical model.
