rat aorta
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Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1997
Author(s):  
Mónika Valdenegro ◽  
Maricarmen Bernales ◽  
Marcela Knox ◽  
Raúl Vinet ◽  
Eduardo Caballero ◽  
...  

The peumo (Cryptocarya alba) is a native fruit from central Chile that belongs to the Lauraceae family. To characterize the development and the potential health benefits of this edible fruit, quality and physiological parameters, along with antioxidant capacity, were evaluated during three clearly defined developmental stages of the fruit in two seasons. The most distinguishable attributes of ripe fruit were the change in size and color. Low CO2 production and no detectable ethylene levels suggested non-climacteric behavior of the peumo fruit. Peumo demonstrate a significant increase in their antioxidant capacity per 1 g of fresh weight (FW) of the sample, from small to ripe fruit. Higher values in ripe fruit (FRAP: 37.1–38.3 µmol FeSO4/gFW, TEAC: 7.9–8.1 mmol TE/gFW, DPPH: 8.4-8.7 IC50 μg/mL, and ORAC: = 0.19–0.20 mmol TE/gFW) were observed than those in blueberry fruit (FRAP: 4.95 µmol FeSO4/gFW, TEAC: 1.25 mmol TE/gFW, DPPH: 11.3 IC50 μg/mL, and ORAC: 0.032 mmol TE/ gFW). The methanol extracts of ripe fruit displayed the presence of polyphenol acids and quercetin, an ORAC value of 0.637 ± 0.061 mmol TE per g dried weight (DW), and a high cellular antioxidant and anti-inflammatory potential, the latter exceeding the effect of quercetin and indomethacin used as standard molecules. Also, the assay of isolated rat aorta with endothelium-dependent relaxation damage demonstrated that the peumo extract induced vascular protection, depending on its concentration under a high glucose condition. These results demonstrate that these endemic fruits have a good chance as ingredients or foods with functional properties.


Author(s):  
Indrani Chakraborty ◽  
Nirmal Chandra Sukul ◽  
Rungrapa Mesripong ◽  
Nattaya Chaothanaphat ◽  
Prasan Dhummaupakorn ◽  
...  

BACKGROUND Homeopathic potencies have been reported to produce alteration of contraction in isolated rat ileum in an organ bath. Potentized homeopathic drugs like Lycopus V and Aurum met are used for the treatment of hypertension. AIM The purpose of this study is to see whether Lycopus V 30 CH and Aurum met 30 CH could produce relaxation of isolated rat aorta in the organ bath. METHODS The aorta of rats were dissected out, placed in Krebs-Henseleit solution, cleared of connective tissue and endothelium and cut into 2-2.5 mm long rings. The rings were fixed in organ baths with the upper end connected by a string to an isometric transducer which was finally attached through a data acquisitation equipment to a computer. Aurum met 30 CH Lycopus V 30 CH, and their medium 90% ethanol were added separately to the bathing fluid containing the aorta rings which were precontracted with noradrenalin (NA). RESULTS Both the drugs produced significant relaxation of the aorta (p


2021 ◽  
Vol 20 (9) ◽  
pp. 1941-1947
Author(s):  
Huawei Tian ◽  
Yuping Li ◽  
Jun Zhang

Purpose: To investigate the effect of leaf extract of Dioscorea deltoidea (Dioscoreaceae) leaf (DDE) on atherosclerosis-induced aorta wall damage in a rat model, and the underlying mechanism of action.Methods: Rats were fed high-fat diet containing vitamin D2 for 16 weeks to induce atherosclerosis. Histopathological changes in the aorta were examined using hematoxylin and eosin (H & E) staining, while ELISA kits were used to measure cytokine levels.Results: Treatment with DDE significantly (p < 0.05) alleviated atherosclerosis-induced increase in mean lesion area in the rat aorta. The mean lesion area in atherosclerotic rats was decreased to 51.5, 21.2 and 2.3 mm2, on treatment with DDE at doses of 2.5, 5 and 10 mg/kg, respectively. Furthermore, DDE significantly suppressed atherosclerosis-induced elevation in IL-1β and IL-6 levels in the rat aorta (p < 0.05). The levels of MCP-1 and TNF-α decreased in the artherosclerotic rats on treatment with DDE. In DDE-treated rats, the atherosclerosis-induced increase in the levels of Ang II, AT1, AT2, p-STAT3, p-p65 and p-p38 were significantly decreased, relative to the model group (p < 0.05). However, DDE treatment did not alter the levels of total STAT3, p65 and p38 in the rat aorta tissues.Conclusion: These results indicate that DDE inhibits inflammatory response and atherosclerosisinduced damage to aorta wall. Moreover, RAAS expression, inflammatory cytokines and JAK/STAT signalling pathway were down-regulated in atherosclerotic rats on treatment with DDE. Thus, DDE may be a potential source of drug for the management of atherosclerosis.


2021 ◽  
pp. 809-813
Author(s):  
K SZMICSEKOVÁ ◽  
L BIES PIVÁČKOVÁ ◽  
Z KILIÁNOVÁ ◽  
L SLOBODOVÁ ◽  
P KŘENEK ◽  
...  

Despite the fact that vessels have sparse cholinergic innervation, acetylcholine (ACh), the primary neurotransmitter of parasympathetic nervous system, has been commonly used in physiological experiments to assess vascular function. ACh is hydrolyzed by two cholinesterases (ChE), namely acetylcholin-esterase and butyrylcholinesterase (BChE). However, little is known about these enzymes in blood vessels. The aim of the project was to characterize the expression and activity of ChE in rat aorta. As the effect of ACh on vascular tone depends on the presence of endothelium, Wistar rats were used as a model with intact endothelium and spontaneously hypertensive rats as a model of impaired endothelial function. Relative expressions of both ChE in different parts of the aorta were determined using RT-qPCR. Enzyme activities were assessed in tissue homogenates by Ellman's assay. Here we showed that both ChE are present in each part of rat aorta, while mRNA is more abundant for BChE than for AChE, irrespective of aortic compartment or genotype. Normotensive Wistar rats possess higher aortic mRNA expression and activity of BChE compared to SHR. We concluded that BChE is the dominant type of ChE in rat aorta and it might play an important role in the regulation of vascular tone


ACS Omega ◽  
2021 ◽  
Author(s):  
Hualong Bai ◽  
Shunbo Wei ◽  
Peng Sun ◽  
Liwei Zhang ◽  
Yuanfeng Liu ◽  
...  
Keyword(s):  

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2548
Author(s):  
Sumukh Thakar ◽  
Yash T Katakia ◽  
Shyam Kumar Ramakrishnan ◽  
Niyati Pandya Pandya Thakkar ◽  
Syamantak Majumder

Epigenetic mechanisms have emerged as one of the key pathways promoting diabetes-associated complications. Herein, we explored the role of enhancer of zeste homolog 2 (EZH2) and its product histone 3 lysine 27 trimethylation (H3K27me3) in high glucose-mediated endothelial inflammation. To examine this, we treated cultured primary endothelial cells (EC) with different treatment conditions—namely, constant or intermittent or transient high glucose. Intermittent high glucose maximally induced endothelial inflammation by upregulating transcript and/or protein-level expression of ICAM1 and P-selectin and downregulating eNOS, KLF2, and KLF4 protein levels. We next investigated the underlining epigenetic mechanisms responsible for intermittent hyperglycemia-dependent endothelial inflammation. Compared with other high glucose treatment groups, intermittent high glucose-exposed EC exhibited an increased level of H3K27me3 caused by reduction in EZH2 threonine 367 phosphorylation and nuclear retention of EZH2. Intermittent high glucose also promoted polycomb repressive complex-2 (PRC2) assembly and EZH2′s recruitment to histone H3. Abrupt enrichment of H3K27me3 on KLF2 and KLF4 gene promoters caused repression of these genes, further supporting endothelial inflammation. In contrast, reducing H3K27me3 through small molecule and/or siRNA-mediated inhibition of EZH2 rescued KLF2 level and inhibited endothelial inflammation in intermittent high glucose-challenged cultured EC and isolated rat aorta. These findings indicate that abrupt chromatin modifications cause high glucose-dependent inflammatory switch of EC.


Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Ji Hye Chun ◽  
Melissa M Henckel ◽  
Leslie A Knaub ◽  
Lori A Walker ◽  
Jane E Reusch ◽  
...  

Cardiovascular disease (CVD) is a leading cause of hospitalization and death. CVD is characterized by impaired vasoreactivity and mitochondrial dysfunction. Perivascular adipose tissue (PVAT), considered brown adipose tissue (BAT), surrounds the vasculature and regulates its response. Preliminary data with rats housed at either their thermoneutrality (TN, 30°C) or room temperature (RT, 22°C) showed diminished vasodilation in aorta from TN rats as compared with those from RT rats (10.2% ± 4.0% (0.159 g of vasodilation capacity, starting from maximal force constriction of 1.563 g) versus 64.2% ± 5.3% (0.909 g of 1.417 g, p<0.001). TN-housed rat aorta also showed less mitochondrial respiration with lipid substrates in multiple states (p<0.05). We hypothesize that remodeling of PVAT phenotype from BAT to white adipose tissue (WAT) may alter mitochondrial lipid utilization and cause vasoreactivity dysfunction. To test this, we housed male and female rats at either RT or TN and investigated their own PVAT + aorta or PVAT from the oppositely- housed animals along with each rat’s own aorta for vasoreactivity ex situ. There was diminished vasodilation in all TN animals with PVAT + aorta (29.2% ± 3.8% (0.269 g of 0.923 g) versus 37.6% ± 6.0% (0.255 g of 0.677 g), p<0.02), with only male animals showing a significant effect from PVAT (p<0.001). In aorta of TN-housed animals analyzed with PVAT from RT-housed animals, female vessels showed an increase in vasodilation capacity as compared to controls (56.8% ± 13.6% (0.589 g of 1.037 g) versus 5.2% ± 2.3% (0.028 g of 0.534 g), p<0.001), strongly suggesting that PVAT not only regulates vasoreactivity, but can repair TN-induced diminished dilation in a sex-dependent manner. All animals at TN had significantly less mitochondrial respiration with lipid substrates (p<0.05), with no sex differences. We further observed a significantly greater amount of lipids in PVAT from male TN-housed animals as compared to that in RT-housed animals (p<0.05), consistent with a WAT phenotype. Our data support that TN alters PVAT phenotype in a sex-dependent manner, resulting in dysfunctional vasoreactivity and mitochondrial function. These targets of CVD in both male and female animals are exciting avenues for novel therapeutics.


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