scholarly journals Betaine and Isoquinoline Alkaloids Protect against Heat Stress and Colonic Permeability in Growing Pigs

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1024 ◽  
Author(s):  
Hieu Huu Le ◽  
Majid Shakeri ◽  
Hafiz Ansar Rasul Suleria ◽  
Weicheng Zhao ◽  
Rachel Mai McQuade ◽  
...  

Heat stress (HS) compromises productivity of pork production, in part as a result of increased oxidative stress and inflammatory responses, particularly within the gastrointestinal tract. This study aimed to investigate whether plant-derived betaine and isoquinoline alkaloids could ameliorate HS in pigs. Fifty female Large White × Landrace grower pigs, which were acclimated to control (CON), control plus betaine (BET), or control plus isoquinoline alkaloids (IQA) diets for 14 days were then exposed to heat stress or thermoneutral condition. Both BET and IQA partially ameliorated increases in respiration rate (p = 0.013) and rectal temperature (p = 0.001) associated with HS conditions. Heat stress increased salivary cortisol concentrations and reduced plasma creatinine, lactate, and thyroid hormone concentrations. Heat stress increased colon FD4 permeability, which was reduced by IQA (p = 0.030). Heat stress increased inflammation in the jejunum and ileum, as indicated by elevated interleukin-1β (p = 0.022) in the jejunum and interleukin-1β (p = 0.004) and interleukin-8 (p = 0.001) in the ileum. No differences in plasma total antioxidant capacity (TAC) were observed with HS, but betaine increased plasma TAC compared to IQA. Dietary BET increased betaine concentrations in the jejunum, ileum (p < 0.001 for both), plasma, liver, kidney (p < 0.010 for all), urine (p = 0.002) and tended to be higher in muscle (p = 0.084). Betaine concentration was not influenced by HS, but it tended to be higher in plasma and accumulated in the liver. These data suggest that betaine and isoquinoline alkaloids supplementation ameliorated consequences of heat stress in grower pigs and protected against HS induced increases in colonic permeability.

2021 ◽  
Vol 12 ◽  
Author(s):  
Ahreum Baek ◽  
So Hee Jung ◽  
Soonil Pyo ◽  
Soo Yeon Kim ◽  
Seongmoon Jo ◽  
...  

Osteoarthritis (OA) is a major degenerative joint disease. Oxidative stress and inflammation play key roles in the pathogenesis of OA. 3′-Sialyllactose (3′-SL) is derived from human milk and is known to regulate a variety of biological functions related to immune homeostasis. This study aimed to investigate the therapeutic mechanisms of 3′-SL in interleukin-1β (IL-1β)-treated SW1353 chondrocytic cells. 3′-SL potently suppressed IL-1β-induced oxidative stress by increasing the levels of enzymatic antioxidants. 3′-SL significantly reversed the IL-1β mediated expression levels of reactive oxygen species in IL-1β-stimulated chondrocytic cells. In addition, 3′-SL could reverse the increased levels of inflammatory markers such as nitrite, prostaglandin E2, inducible nitric oxide synthase, cyclooxygenase-2, IL-1β, and IL-6 in IL-1β-stimulated chondrocytic cells. Moreover, 3′-SL significantly inhibited the apoptotic process, as indicated by the downregulation of the pro-apoptotic protein Bax, upregulation of the anti-apoptotic protein Bcl-2 expression, and significant reduction in the number of TUNEL-positive cells in the IL-1β-treated chondrocytic cells. Furthermore, 3′-SL reversed cartilage destruction by decreasing the release of matrix metalloproteinases (MMP), such as MMP1, MMP3, and MMP13. In contrast, 3′-SL significantly increased the expression levels of matrix synthesis proteins, such as collagen II and aggrecan, in IL-1β-treated chondrocytic cells. 3′-SL dramatically suppressed the activation of mitogen-activated protein kinases (MAPK) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways, which are related to the pathogenesis of OA. Taken together, our data suggest that 3′-SL alleviates IL-1β-induced OA pathogenesis via inhibition of activated MAPK and PI3K/AKT/NF-κB signaling cascades with the downregulation of oxidative stress and inflammation. Therefore, 3′-SL has the potential to be used as a natural compound for OA therapy owing to its ability to activate the antioxidant defense system and suppress inflammatory responses.


Animals ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 359 ◽  
Author(s):  
Wei Fang ◽  
Xiaobin Wen ◽  
Qingshi Meng ◽  
Lei Liu ◽  
Jingjing Xie ◽  
...  

Heat stress influences lipid metabolism independently of nutrient intake. It is not well understood how cholesterol and bile acid (BA) metabolism are affected by heat stress. To investigate the alterations of cholesterol and bile acids when pigs are exposed to short term heat stress, 24 Large White pigs (63.2 ± 9.5 kg body weight, BW) were distributed into one of three environmental treatments: control conditions (CON, 23 °C with ad libitum intake; n = 8), heat stress conditions (HS, 33 °C with ad libitum intake; n = 8), or pair-fed conditions (PF, 23 °C with the same amount to the feed consumed by the HS; n = 8) for three days. Compared with CON pigs, HS pigs reduced the average daily feed intake and average daily gain by 55% and 124%, respectively, and significantly increased rectal temperatures by 0.9 °C and respiration rates more than three-fold. The serum total cholesterol (TC), low-density lipoprotein-cholesterol, and triglycerides (TG) increased (p < 0.05), while hepatic TC, TG, and mRNA of 3-hydroxy-3-methylglutaryl-CoA reductase were reduced on day 3. Furthermore, liver taurine-conjugated BAs (TCBAs), including taurolithocholic acid, taurochenodeoxycholic acid (TCDCA), tauroursodeoxycholic acid, taurohyodeoxycholic acid, and taurocholic acid were elevated in HS pigs compared to CON and PF pigs (p < 0.05), and the level of chenodeoxycholic acid was more significant in the PF group than in the CON and HS groups. The concentration of ursodeoxycholic acid in the serum was higher in HS pigs than CON and PF pigs (p < 0.05), and TCDCA was increased in HS pigs compared with PF pigs (p < 0.05). Altogether, short-term HS reduced hepatic cholesterol levels by decreasing cholesterol synthesis, promoting cholesterol to TCBAs conversion, and cholesterol release to serum in growing pigs. This independently reduced feed intake might serve as a mechanism to protect cells from damage during the early period.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Na Qiao ◽  
Hanming Chen ◽  
Peiquan Du ◽  
Zhenlong Kang ◽  
Congying Pang ◽  
...  

Acetyl-L-carnitine (ALC) is an effective substrate for mitochondrial energy metabolism and is known to prevent neurodegeneration and attenuate heavy metal-induced injury. In this study, we investigated the function of ALC in the recovery of mouse spermatogonia cells (GC-1 cells) after heat stress (HS). The cells were randomly divided into three groups: control group, HS group (incubated at 42°C for 90 min), and HS + ALC group (treatment of 150 μM ALC after incubated at 42°C for 90 min). After heat stress, all of the cells were recovered at 37°C for 6 h. In this study, the content of intracellular lactate dehydrogenase (LDH) in the cell supernatant and the malondialdehyde (MDA) levels, catalase (CAT) levels, and total antioxidant capacity (T-AOC) were significantly increased in the HS group compared to the CON group. In addition, the mitochondrial membrane potential (MMP) was markedly decreased, while the apoptosis rate and the expression of apoptosis-related genes (Bcl-2, Bax, and caspase3) were significantly increased in the HS group compared to the CON group. Furthermore, the number of autophagosomes and the expression of autophagy-related genes (Atg5, Beclin1, and LC3II) and protein levels of p62 were increased, but the expression of LAMP1 was decreased in the HS group compared to the CON group. However, treatment with ALC remarkably improved cell survival and decreased cell oxidative stress. It was unexpected that levels of autophagy were markedly increased in the HS + ALC group compared to the HS group. Taken together, our present study evidenced that ALC could alleviate oxidative stress and improve the level of autophagy to accelerate the recovery of GC-1 cells after heat stress.


Molecules ◽  
2020 ◽  
Vol 25 (5) ◽  
pp. 1019 ◽  
Author(s):  
Sungwoo Chei ◽  
Ji-Hyeon Song ◽  
Hyun-Ji Oh ◽  
Kippeum Lee ◽  
Heegu Jin ◽  
...  

Heat stress can be caused by various environmental factors. When exposed to heat stress, oxidative stress and inflammatory reaction occur due to an increase of reactive oxygen species (ROS) in the body. In particular, inflammatory responses induced by heat stress are common in muscle cells, which are the most exposed to heat stress and directly affected. Gintonin-Enriched Fraction (GEF) is a non-saponin component of ginseng, a glycolipoprotein. It is known that it has excellent neuroprotective effects, therefore, we aimed to confirm the protective effect against heat stress by using GEF. C2C12 cells were exposed to high temperature stress for 1, 12 and 15 h, and the expression of signals was analyzed over time. Changes in the expression of the factors that were observed under heat stress were confirmed at the protein level. Exposure to heat stress increases phosphorylation of p38 and extracellular signal-regulated kinase (ERK) and increases expression of inflammatory factors such as NLRP3 inflammasome through lysophosphatidic acid (LPA) receptor. Activated inflammatory signals also increase the secretion of inflammatory cytokines such as interleukin 6 (IL-6) and interleukin 18 (IL-18). Also, expression of glutathione reductase (GR) and catalase related to oxidative stress is increased. However, it was confirmed that the changes due to the heat stress were suppressed by the GEF treatment. Therefore, we suggest that GEF helps to protect heat stress in muscle cell and prevent tissue damage by oxidative stress and inflammation.


2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 179-179
Author(s):  
Hieu H Le ◽  
Eva Vidacs ◽  
Deborah J Phillips ◽  
Weicheng Zhao ◽  
John B Furness ◽  
...  

Abstract Heat stress (HS) compromises efficient production of pigs, in part by increasing oxidative stress and inflammation. Therefore the aim of this experiment was to investigate if supplementation of the anti-oxidants selenium or superoxide dismutase (SOD) could ameliorate HS in the pig. Sixty-four female Large White x Landrace pigs (av. 27.75) were acclimated one of the following diets: control (standard grower diet), selenium (Se, + 0.3 ppm organic Se), recombinant SOD (rSOD, 50 IU/d) and Se plus rSOD (SS) for 14 days under thermoneutral conditions (TN, 200C). All rSOD was administered top dressed in liquid form. Pigs were then moved to climate rooms and housed under TN or heat-stress (8 h 350C, 16h 280C/d) for 3 days and blood, urine and tissue collected for analysis terminally on d3. All data was analysed using an ANOVA with Tukeys post-hoc tests. Heat stress increased respiration rate (RR), reduced blood pCO2 and HCO3-, which coupled with a lower base excess indicated that the pigs were experiencing respiratory alkalosis. Furthermore HS increased rectal and skin temperatures, and reduced thyroid hormone (T4) concentrations, however HSP 27 and 70 concentrations were not influenced. Heat stress increased plasma adiponectin and IL-1b, reduced SOD and TNF-a, while no changes in IL-6 and leptin were observed. The effects of the anti-oxidant diets were that Se and SS increased RR, however parameters of respiratory alkalosis were not negatively influenced. The Se diet reduced T4 independently of HS. No improvement in plasma SOD was observed with the rSOD diets, but rSOD reduced adiponectin in HS pigs and both rSOD and SS reduced IL-6 overall. In conclusion a reduction in inflammatory responses were observed with the antioxidants Se and rSOD, including during HS and therefore may be a useful addition to existing amelioration strategies to ameliorate seasonal heat stress in pigs.


Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.


1999 ◽  
Vol 82 (S 01) ◽  
pp. 32-37 ◽  
Author(s):  
Karlheinz Peter ◽  
Wolfgang Kübler ◽  
Johannes Ruef ◽  
Thomas K. Nordt ◽  
Marschall S. Runge ◽  
...  

SummaryThe initiating event of atherogenesis is thought to be an injury to the vessel wall resulting in endothelial dysfunction. This is followed by key features of atherosclerotic plaque formation such as inflammatory responses, cell proliferation and remodeling of the vasculature, finally leading to vascular lesion formation, plaque rupture, thrombosis and tissue infarction. A causative relationship exists between these events and oxidative stress in the vessel wall. Besides leukocytes, vascular cells are a potent source of oxygen-derived free radicals. Oxidants exert mitogenic effects that are partially mediated through generation of growth factors. Mitogens, on the other hand, are potent stimulators of oxidant generation, indicating a putative self-perpetuating mechanism of atherogenesis. Oxidants influence the balance of the coagulation system towards platelet aggregation and thrombus formation. Therapeutic approaches by means of antioxidants are promising in both experimental and clinical designs. However, additional clinical trials are necessary to assess the role of antioxidants in cardiovascular disease.


2019 ◽  
Vol 70 (8) ◽  
pp. 2822-2825 ◽  
Author(s):  
Cornel Moisa ◽  
Mihnea Alexandru Gaman ◽  
Camelia Cristina Diaconu ◽  
Amelia Maria Gaman

Essential thrombocythemia (ET) is a BCR-ABL1-negative myeloproliferative neoplasm associated with thrombotic and haemorrhagic complications. Reactive oxygen species (ROS) overexpression induces a growth advantage to JAK2V617F-positive clones and, in association with a higher number of immature platelets, leukocytosis, and additional cardiovascular risk factors, leads to an increased risk for thrombotic events. We evaluated oxidative stress by measuring ROS levels and the total antioxidant capacity (TAC) in 62 ET patients and investigated the relationship between oxidative stress, JAK2V617F mutational status and the development of thrombotic events. We found higher oxidative stress levels in JAK2V617F-positive vs. JAK2V617F-negative ET cases with no significant differences between homozygous and heterozygous genotypes. Increased ROS levels and thrombotic events were more frequent in ET patients with old age at diagnosis, higher haematocrit levels or leukocytosis.


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