scholarly journals Bisdemethoxycurcumin Protects Small Intestine from Lipopolysaccharide-Induced Mitochondrial Dysfunction via Activating Mitochondrial Antioxidant Systems and Mitochondrial Biogenesis in Broiler Chickens

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Jingfei Zhang ◽  
Yuxiang Yang ◽  
Hongli Han ◽  
Lili Zhang ◽  
Tian Wang
Keyword(s):  
Mitochondrial Dysfunction ◽  
Mitochondrial Biogenesis ◽  
Broiler Chickens ◽  
Manganese Superoxide Dismutase ◽  
Antioxidant Systems ◽  
Sterile Saline ◽  
Lps Challenge ◽  
Mitochondrial Dna Copy Number ◽  
Small Intestinal ◽  
Thioredoxin 2

Bisdemethoxycurcumin is one of the three curcuminoids of turmeric and exhibits good antioxidant activity in animal models. This study is aimed at investigating the effect of bisdemethoxycurcumin on small intestinal mitochondrial dysfunction in lipopolysaccharide- (LPS-) treated broilers, especially on the mitochondrial thioredoxin 2 system and mitochondrial biogenesis. A total of 320 broiler chickens were randomly assigned into four experimental diets using a 2 × 2 factorial arrangement with diet (0 and 150 mg/kg bisdemethoxycurcumin supplementation) and stress (saline or LPS challenge) for 20 days. Broilers received a dose of LPS (1 mg/kg body weight) or sterile saline intraperitoneally on days 16, 18, and 20 of the trial. Bisdemethoxycurcumin mitigated the mitochondrial dysfunction of jejunum and ileum induced by LPS, as evident by the reduced reactive oxygen species levels and the increased mitochondrial membrane potential. Bisdemethoxycurcumin partially reversed the decrease in the mitochondrial DNA copy number and the depletion of ATP levels. Bisdemethoxycurcumin activated the mitochondrial antioxidant response, including the prevention of lipid peroxidation, enhancement of manganese superoxide dismutase activity, and the upregulation of the mitochondrial glutaredoxin 5 and thioredoxin 2 system. The enhanced mitochondrial respiratory complex activities in jejunum and ileum were also attributed to bisdemethoxycurcumin treatment. In addition, bisdemethoxycurcumin induced mitochondrial biogenesis via transcriptional regulation of proliferator-activated receptor-gamma coactivator-1alpha pathway. In conclusion, our results demonstrated the potential of bisdemethoxycurcumin to attenuate small intestinal mitochondrial dysfunction, which might be mediated via activating the mitochondrial antioxidant system and mitochondrial biogenesis in LPS-treated broilers.

Effects of an early lipopolysaccharide challenge on growth and small intestinal structure and function of broiler chickens

2011 ◽  
Vol 91 (3) ◽  
pp. 379-384 ◽  
Author(s):  
Xiao Hu ◽  
Yu Guo ◽  
Jian Li ◽  
Gui Yan ◽  
Sideoun Bun ◽  
...  
Keyword(s):  
Small Bowel ◽  
Broiler Chickens ◽  
Mrna Level ◽  
Structure And Function ◽  
Labeling Index ◽  
Villus Height ◽  
Lps Challenge ◽  
Intestinal Peristalsis ◽  
Small Intestinal ◽  
And Function

Hu, X. F., Guo, Y. M., Li, J. H., Yan, G. L., Bun, S. and Huang, B. Y. 2011. Effects of an early lipopolysaccharide challenge on growth and small intestinal structure and function of broiler chickens. Can. J. Anim. Sci. 91: 379–384. Two experiments were conducted to determine the effect of early exposure to lipopolysaccharide (LPS) on small intestinal structure and function of broiler chickens. Seven-day-old birds were randomly allotted to two equal treatments: an LPS-injected treatment in which the birds were injected intraperitoneally with LPS 500 µg kg−1 body weight (dissolved in 1 mL saline) on 8, 10, 12, 15, 17, and 19 d of age, i.e., on days 1, 3, and 5 d for 2 continuous weeks, and a control treatment (CTRL) in which the birds were similarly injected with 1 mL saline as a placebo. In exp. 1, food intake and weight gain were monitored over the 2 wk, the weight of the small bowel was determined at 14 and 21 d of age and duodenal and jejunal villus height and crypt depth, D-xylose uptake were also measured at 21 d. In exp. 2, additional measurements of the intestinal peristalsis ratio and the BrdU-labeling index and duodenal sodium-glucose co-transporter-1 (SGLT1) mRNA level were made at 21 d of age. The results showed that LPS challenge decreased feed intake, daily gain, duodenal and jejunal villus height and crypt depth, plasma D-xylose concentration and intestinal BrdUrd-labeling index, respectively (P<0.05) as well as small bowel weight at 14 and 21 d of age (P<0.05). Conversely, LPS injection increased SGLT1 mRNA level in the small intestine (P<0.05) and the small intestinal relative weight at 14 (P<0.05) and 21 d of age (P=0.063). Following LPS injection there were non-significant changes in feed conversion ratio and intestinal peristalsis ratio (P>0.05). In conclusion, early LPS challenge delayed the growth of intestine and impaired small intestinal structure and absorptive function.

scholarly journals One Week of CDAHFD Induces Steatohepatitis and Mitochondrial Dysfunction with Oxidative Stress in Liver

2021 ◽  
Vol 22 (11) ◽  
pp. 5851
Author(s):  
Takehito Sugasawa ◽  
Seiko Ono ◽  
Masato Yonamine ◽  
Shin-ichiro Fujita ◽  
Yuki Matsumoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Early Stage ◽  
Droplet Deposition ◽  
Nonalcoholic Fatty Liver ◽  
Stress Markers ◽  
Mitochondrial Dna Copy Number ◽  
Short Period ◽  
And Oxidative Stress

The prevalence of nonalcoholic fatty liver disease (NAFLD) has been rapidly increasing worldwide. A choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) has been used to create a mouse model of nonalcoholic steatohepatitis (NASH). There are some reports on the effects on mice of being fed a CDAHFD for long periods of 1 to 3 months. However, the effect of this diet over a short period is unknown. Therefore, we examined the effect of 1-week CDAHFD feeding on the mouse liver. Feeding a CDAHFD diet for only 1-week induced lipid droplet deposition in the liver with increasing activity of liver-derived enzymes in the plasma. On the other hand, it did not induce fibrosis or cirrhosis. Additionally, it was demonstrated that CDAHFD significantly impaired mitochondrial respiration with severe oxidative stress to the liver, which is associated with a decreasing mitochondrial DNA copy number and complex proteins. In the gene expression analysis of the liver, inflammatory and oxidative stress markers were significantly increased by CDAHFD. These results demonstrated that 1 week of feeding CDAHFD to mice induces steatohepatitis with mitochondrial dysfunction and severe oxidative stress, without fibrosis, which can partially mimic the early stage of NASH in humans.

scholarly journals Interactions between starch source and gelatinisation degree on performance and small intestinal digestion in broiler chickens

2021 ◽  
pp. 1-11
Author(s):  
K. Itani ◽  
J. Ø. Hansen ◽  
B. Kierończyk ◽  
A. Benzertiha ◽  
P. P. Kurk ◽  
...  
Keyword(s):  
Broiler Chickens ◽  
Intestinal Digestion ◽  
Small Intestinal

scholarly journals INFECTIOUS STUNTING SYNDROME ASSOCIATED WITH DISTURBANCES OF MINERAL METABOLISM AND BONE DEVELOPMENT IN BROILER CHICKENS

1999 ◽  
Vol 47 (3) ◽  
pp. 361-378 ◽  
Author(s):  
Glávits ◽  
G. Sályi ◽  
R. Glávits
Keyword(s):  
Growth Retardation ◽  
Broiler Chickens ◽  
Neuronal Degeneration ◽  
Bone Development ◽  
Mineral Metabolism ◽  
Digestive Enzyme ◽  
Small Intestinal Mucosa ◽  
Vacuolar Degeneration ◽  
Leg Weakness ◽  
Small Intestinal

On a broiler farm with a rearing capacity of about 200,000 chickens, a disease characterised by growth retardation, variability in chick size, 'leg weakness', diarrhoea and increased mortality at 3 weeks of age occurred repeatedly, in several successive broiler flocks. Gross and histopathological findings were dominated by widening of the hypertrophic and ossification layers of the physes of long bones as well as by thickening, unevenness and defective calcification of the cartilage trabeculae. In the parathyroid gland, vacuolar degeneration of the cytoplasm of glandular epithelial cells, connective tissue proliferation and, here and there, cyst formation were seen. Additional findings included severe cerebellar oedema and neuronal degeneration. The pancreatic, myocardial and intestinal changes typical of infectious stunting syndrome (ISS) occurred only in a mild form. Four-week-old chickens exhibiting 'leg weakness' had significantly lower blood inorganic phosphate concentration and tibial ash content as compared to healthy chickens. The disease was successfully transmitted by oral administration of small intestinal homogenate from affected chickens. In a second experiment, however, the disease could not be transmitted with intestinal homogenate sterilized by irradiation. Large doses of vitamin D3reduced the rate of growth retardation and defective calcification of bones. The digestive enzyme activities of the pancreas and small intestinal mucosa of 'infected' chickens were decreased as is typical of ISS.

scholarly journals Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities

2021 ◽  
Vol 12 ◽  
Author(s):  
Paulo H. C. Mesquita ◽  
Christopher G. Vann ◽  
Stuart M. Phillips ◽  
James McKendry ◽  
Kaelin C. Young ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Mitochondrial Biogenesis ◽  
Ribosome Biogenesis ◽  
Exercise Physiology ◽  
Future Research ◽  
Mitochondrial Dna Copy Number ◽  
Mtorc1 Signaling ◽  
Amp Activated Protein Kinase ◽  
Training Modalities

Skeletal muscle adaptations to resistance and endurance training include increased ribosome and mitochondrial biogenesis, respectively. Such adaptations are believed to contribute to the notable increases in hypertrophy and aerobic capacity observed with each exercise mode. Data from multiple studies suggest the existence of a competition between ribosome and mitochondrial biogenesis, in which the first adaptation is prioritized with resistance training while the latter is prioritized with endurance training. In addition, reports have shown an interference effect when both exercise modes are performed concurrently. This prioritization/interference may be due to the interplay between the 5’ AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin complex 1 (mTORC1) signaling cascades and/or the high skeletal muscle energy requirements for the synthesis and maintenance of cellular organelles. Negative associations between ribosomal DNA and mitochondrial DNA copy number in human blood cells also provide evidence of potential competition in skeletal muscle. However, several lines of evidence suggest that ribosome and mitochondrial biogenesis can occur simultaneously in response to different types of exercise and that the AMPK-mTORC1 interaction is more complex than initially thought. The purpose of this review is to provide in-depth discussions of these topics. We discuss whether a curious competition between mitochondrial and ribosome biogenesis exists and show the available evidence both in favor and against it. Finally, we provide future research avenues in this area of exercise physiology.

scholarly journals DNA Methylation of PGC-1α Is Associated With Elevated mtDNA Copy Number and Altered Urinary Metabolites in Autism Spectrum Disorder

2021 ◽  
Vol 9 ◽  
Author(s):  
Sophia Bam ◽  
Erin Buchanan ◽  
Caitlyn Mahony ◽  
Colleen O’Ryan
Keyword(s):  
Autism Spectrum Disorder ◽  
Dna Methylation ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Copy Number ◽  
Autism Spectrum ◽  
Differential Methylation ◽  
Mtdna Copy Number ◽  
Key Genes

Autism spectrum disorder (ASD) is a complex disorder that is underpinned by numerous dysregulated biological pathways, including pathways that affect mitochondrial function. Epigenetic mechanisms contribute to this dysregulation and DNA methylation is an important factor in the etiology of ASD. We measured DNA methylation of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α), as well as five genes involved in regulating mitochondrial homeostasis to examine mitochondrial dysfunction in an ASD cohort of South African children. Using targeted Next Generation bisulfite sequencing, we found differential methylation (p &lt; 0.05) at six key genes converging on mitochondrial biogenesis, fission and fusion in ASD, namely PGC-1α, STOML2, MFN2, FIS1, OPA1, and GABPA. PGC-1α, the transcriptional regulator of biogenesis, was significantly hypermethylated at eight CpG sites in the gene promoter, one of which contained a putative binding site for CAMP response binding element 1 (CREB1) (p = 1 × 10–6). Mitochondrial DNA (mtDNA) copy number, a marker of mitochondrial function, was elevated (p = 0.002) in ASD compared to controls and correlated significantly with DNA methylation at the PGC-1α promoter and there was a positive correlation between methylation at PGC-1α CpG#1 and mtDNA copy number (Spearman’s r = 0.2, n = 49, p = 0.04) in ASD. Furthermore, DNA methylation at PGC-1α CpG#1 and mtDNA copy number correlated significantly (p &lt; 0.05) with levels of urinary organic acids associated with mitochondrial dysfunction, oxidative stress, and neuroendocrinology. Our data show differential methylation in ASD at six key genes converging on PGC-1α-dependent regulation of mitochondrial biogenesis and function. We demonstrate that methylation at the PGC-1α promoter is associated with elevated mtDNA copy number and metabolomic evidence of mitochondrial dysfunction in ASD. This highlights an unexplored role for DNA methylation in regulating specific pathways involved in mitochondrial biogenesis, fission and fusion contributing to mitochondrial dysfunction in ASD.

scholarly journals Dexmedetomidine Attenuates Lung Ischemia-reperfusion Injury in Rats by Reducing Mitochondrial Dysfunction

2020 ◽  
Author(s):  
Yan Zhang ◽  
Yao Lu ◽  
Kai Wang ◽  
Mei-yan Zhou ◽  
Cong-you Wu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Reperfusion Injury ◽  
Mitochondrial Biogenesis ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Weight Ratio ◽  
Oxygenation Index ◽  
Lung Damage ◽  
Peroxisome Proliferator ◽  
Sprague Dawley

Abstract Background: Lung ischemia-reperfusion injury (LIRI) is a significant clinical problem occurring after lung transplantation. LIRI is mediated by the overproduction of reactive oxygen species (ROS) and inflammatory activation. Previous studies have confirmed that dexmedetomidine (DEX) exerts a protective effect on LIRI, which potentially causes severe mitochondrial dysfunction. However, the specific mechanisms remain unclear. Our study was to explore whether dexmedetomidine exerts a beneficial effect on LIRI by reducing mitochondrial dysfunction. Methods: Two different models were used in our study. For the in vivo experiment, thirty-two male Sprague-Dawley rats were randomly divided into Sham, ischemia-reperfusion (I/R), DEX+I/R and DEX+yohimbine+I/R (DY+I/R) groups. Similarly, pulmonary vascular endothelial cells (PVECs) from SD rats were divided into Control, oxygen glucose deprivation (OGD), D+OGD and DY+OGD groups.Results: In our experiment, we confirmed severe lung damage after LIRI that was characterized by significantly pulmonary histopathology injury, a decrease in the oxygenation index (PaO2/FiO2) and an increase in the wet-to-dry weight ratio, while DEX treatment mitigated this damage. In addition, the DEX pretreatment significantly attenuated I/R-induced oxidative stress by decreasing the level of ROS in the mitochondria in vitro. Moreover, the DEX treatment enhanced mitochondrial biogenesis and autophagy by increasing the expression of peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α), mitochondrial transcription factor A (Tfam), PTEN-induced putative kinase 1 (PINK1), Parkin and dynamin 1-like protein 1 (Drp1). Conclusions: These data suggest that DEX may alleviate LIRI by reducing mitochondrial dysfunction through the induction of mitochondrial biogenesis and autophagy.

Abstract P608: Obesity Induced Hypertension Exacerbated Through Upregulation Of Renal Naci Cotransporter, Reversed By Increasing Pgc-1α-ho-1 Gene Expression To Restore Mitochondrial Function

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
David Bamshad ◽  
Jian Cao ◽  
Joseph Schragenheim ◽  
Charles T Stier ◽  
Nader G Abraham
Keyword(s):  
Mitochondrial Dysfunction ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Sodium Excretion ◽  
Leptin Receptor ◽  
Insulin Receptors ◽  
Urinary Sodium Excretion ◽  
Induced Hypertension ◽  
Group A ◽  
Group B

Introduction: Hypertension caused by chronic obesity as a result of high calorie food intake or in leptin receptor deficient db/db mice may be linked to mitochondrial dysfunction. Previously we and others have shown that an epoxyeicosatrienoic acid agonist (EET-A), reduced adiposity and ROS resulting in normalization of BP by unknown mechanisms. We hypothesize that EET-A will attenuate BP by restoring mitochondrial function through increasing the PGC-1α-HO-1 axis and increasing urinary sodium excretion by downregulating NCC channels. Methods: Db/db mice at 16-wks of age were divided into 3 treatment groups and for an additional 16-wks received: A) control, B) EET-A 1.5mg/100g BW i.p. 2x/week and C) EET-A and lentiviral (Ln)- PGC-1α shRNA (to suppress PGC-1α protein). Oxygen consumption (VO 2 ), visceral fat and blood glucose were determined. Additionally, renal tissues were harvested to measure the type 2 Na-K-Cl cotransporters (NKCC2), epithelial Na channels- (ENaC), NaCl cotransporters (NCC), PGC-1α, HO-1, insulin receptors, and mitochondrial biogenesis markers. Results: At the conclusion of 32 weeks: Group A, developed hypertension and presented with decreased urinary Na excretion, decreased VO 2 , decreased downstream PGC-1α signaling, and mitochondrial dysfunction. There were increased levels of NCCs but not of NKCC2s or ENaCs. Renal PGC-1α, HO-1, pAMPK, and mitochondrial fusion protein Mfn 1/2, and Opa1 were decreased, p<0.05. Group B, exhibited restoration of renal levels of PGC-1α, HO-1, pAMPK, and mitochondrial biogenesis proteins Mfn 1/2 and Opa1. NCC expression was reduced and was associated with an increase in urinary Na excretion; (p<0.05). The beneficial effect of EET-A observed in group B was suppressed in group C using Ln- PGC-1α shRNA which suppressed PGC-1α expression in renal tissue > 50% and was accompanied by the onset of even more severe suppression of urinary Na excretion than in Group A. Conclusion: Treatment of obese mice with EET-agonists leads to the recruitment of PGC-1α-HO-1 which enhances mitochondrial function and induces the downregulation of NCC channels and increased sodium excretion. EET may serve as a powerful therapeutic agent for the treatment of obesity induced hypertension.

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