Selenium exerts protective effects against heat stress induced barrier disruption and inflammation response in jejunum of growing pigs

2021 ◽  
Author(s):  
Ying He ◽  
Yan Liu ◽  
Jiayong Tang ◽  
Gang Jia ◽  
Guangmang Liu ◽  
...  
Keyword(s):  
Heat Stress ◽  
Growing Pigs ◽  
Protective Effects ◽  
Inflammation Response ◽  
Barrier Disruption

scholarly journals Heat Stress Reduces Metabolic Rate While Increasing Respiratory Exchange Ratio in Growing Pigs

Animals ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 215
Author(s):  
Dane W. Fausnacht ◽  
Kellie A. Kroscher ◽  
Ryan P. McMillan ◽  
Luciane S. Martello ◽  
Lance H. Baumgard ◽  
...  
Keyword(s):  
Heat Stress ◽  
Energy Expenditure ◽  
Metabolic Rate ◽  
Respiratory Exchange Ratio ◽  
Muscle Growth ◽  
Growing Pigs ◽  
Metabolic Phenotype ◽  
Substrate Regulation ◽  
Enclosed Chamber ◽  
Muscle Biopsies

Heat stress (HS) diminishes animal production, reducing muscle growth and increasing adiposity, especially in swine. Excess heat creates a metabolic phenotype with limited lipid oxidation that relies on aerobic and anaerobic glycolysis as a predominant means of energy production, potentially reducing metabolic rate. To evaluate the effects of HS on substrate utilization and energy expenditure, crossbred barrows (15.2 ± 2.4 kg) were acclimatized for 5 days (22 °C), then treated with 5 days of TN (thermal neutral, 22 °C, n = 8) or HS (35 °C, n = 8). Pigs were fed ad libitum and monitored for respiratory rate (RR) and rectal temperature. Daily energy expenditure (DEE) and respiratory exchange ratio (RER, CO2:O2) were evaluated fasted in an enclosed chamber through indirect calorimetry. Muscle biopsies were obtained from the longissimus dorsi pre/post. HS increased temperature (39.2 ± 0.1 vs. 39.6 ± 0.1 °C, p < 0.01) and RER (0.91 ± 0.02 vs. 1.02 ± 0.02 VCO2:VO2, p < 0.01), but decreased DEE/BW (68.8 ± 1.7 vs. 49.7 ± 4.8 kcal/day/kg, p < 0.01) relative to TN. Weight gain (p = 0.80) and feed intake (p = 0.84) did not differ between HS and TN groups. HS decreased muscle metabolic flexibility (~33%, p = 0.01), but increased leucine oxidation (~35%, p = 0.02) compared to baseline values. These data demonstrate that HS disrupts substrate regulation and energy expenditure in growing pigs.

scholarly journals PSV-1 Effects of dietary oils on nutrient digestibility in the growing pigs under heat stress condition.

2018 ◽  
Vol 96 (suppl_3) ◽  
pp. 44-44
Author(s):  
W Yun ◽  
J Lee ◽  
C Lee ◽  
W Kwak ◽  
H Oh ◽  
...  
Keyword(s):  
Heat Stress ◽  
Stress Condition ◽  
Nutrient Digestibility ◽  
Growing Pigs ◽  
Dietary Oils ◽  
Heat Stress Condition

Prior heat stress enhances survival of renal epithelial cells after ATP depletion

1996 ◽  
Vol 270 (6) ◽  
pp. F1057-F1065 ◽  
Author(s):  
Y. H. Wang ◽  
S. C. Borkan
Keyword(s):  
Heat Stress ◽  
Epithelial Cells ◽  
Recovery Period ◽  
Atp Depletion ◽  
Protective Effects ◽  
Atp Content ◽  
Renal Epithelial Cells ◽  
Opossum Kidney ◽  
Ok Cells

The 72-kDa heat stress protein (HSP-72) is an inducible cytoprotectant protein. Although transient renal ischemia in vivo induces HSP-72, it is not known whether prior heat stress protects renal epithelial cells from injury mediated by ATP depletion. To evaluate this hypothesis, opossum kidney (OK) cells were exposed to sodium cyanide and 2-deoxy-D-glucose in the absence of medium glucose, a maneuver that reduced cell ATP content to < 10% of the control value within 10 min and decreased cell survival. One day after 2 h of ATP depletion, OK cells previously exposed to heat stress (to induce accumulation of HSP-72) exhibited marked improvement in survival (a > 4-fold increase in total DNA), less uptake of vital dye, and less release of lactate dehydrogenase (LDH) than cells subjected to ATP depletion alone (23.0 +/- 1.6 vs. 34.1 +/- 1.2% of total LDH, respectively). Enhanced clonogenicity post-heat stress was completely prevented by cycloheximide and positively correlated with the steady-state content of HSP-72. In the recovery period after ATP depletion, cell ATP content, maximum mitochondrial ATP production rate, and total LDH activity were all significantly higher in cells with abundant HSP-72. Although the protective effects associated with heat stress are likely to be multifactoral, preserved cell metabolism and higher ATP content could enhance cellular repair processes after ATP depletion.

scholarly journals 235 Effects of rapamycin during an acute heat stress exposure in growing pigs

2020 ◽  
Vol 98 (Supplement_3) ◽  
pp. 117-117
Author(s):  
Edith J Mayorga ◽  
Erin A Horst ◽  
Brady M Goetz ◽  
Sonia Rodríguez-Jiménez ◽  
Megan A Abeyta ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Heat Stress ◽  
Rectal Temperature ◽  
Blood Cells ◽  
White Blood Cells ◽  
Growing Pigs ◽  
Stress Exposure ◽  
Esterified Fatty Acids ◽  
Acute Heat Stress ◽  
Ad Libitum

Abstract Objectives were to determine the effects of rapamycin on biomarkers of metabolism and inflammation during acute heat stress (HS) in growing pigs. Crossbred barrows (n=32; 63.5±0.8 BW) where blocked by BW and randomly assigned to 1 of 4 therapeutic-environmental treatments: 1) thermoneutral (TN) control (n=8; TNCtl), 2) TN and rapamycin (n=8; TNRapa), 3) HS control (n=8; HSCtl), or 4) HS and rapamycin (n=8; HSRapa). The trial consisted of 2 experimental periods (P). During P1 (10d), pigs were fed ad libitum and housed in TN conditions (21.3±0.01°C). During P2 (24h), HSCtl and HSRapa pigs were exposed to constant HS (35.5±0.1°C); while TNCtl and TNRapa remained in TN conditions. Rapamycin (0.15 mg/kg BW) was orally administered twice daily (0700 and 1800 h) during P1 and P2. HS increased rectal temperature, skin temperature, and respiration rate compared to TN counterparts (1.28°C, 8.68°C, and 87 bpm, respectively; P&lt; 0.01). Feed intake (FI) markedly decreased in HS relative to TN treatments (64%; P&lt; 0.01). Additionally, pigs exposed to HS lost BW (4 kg; P&lt; 0.01), while TN pigs gained BW (0.7 kg; P&lt; 0.01). Overall, circulating white blood cells decreased in HS compared to TN pigs (19%; P=0.01). Circulating neutrophils did not differ across treatments; however, lymphocytes, monocytes, and basophils decreased in HS relative to TN pigs (23, 33, and 38%, respectively; P≤0.07). Despite marked changes in phenotypic parameters, circulating glucose and blood urea nitrogen did not differ among treatments (P &gt;0.10). However, insulin:FI increased in HS relative to TN treatments (P=0.04). Plasma non-esterified fatty acids (NEFA) increased in HS relative to TN treatments; although this difference was driven by increased NEFA in HSCtl compared to TN and HSRapa pigs (P&lt; 0.01). In summary, pigs exposed to HS had altered phenotypic, metabolic, and leukocyte responses; however, rapamycin administration had little to no effect on any of the variables measured.

scholarly journals Correction to: Heat stress-induced renal damage in poultry and the protective effects of HSP60 and HSP47

2020 ◽  
Vol 25 (2) ◽  
pp. 379-379
Author(s):  
Shu Tang ◽  
Shuang Zhou ◽  
Bin Yin ◽  
Jiao Xu ◽  
Liangjiao Di ◽  
...  
Keyword(s):  
Heat Stress ◽  
Renal Damage ◽  
Protective Effects

scholarly journals To Provide a Double Feeder in Growing Pigs Housed under High Environmental Temperatures Reduces Social Interactions but Does Not Improve Weight Gains

Animals ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 2248
Author(s):  
Tâmara Duarte Borges ◽  
Mariana Huerta-Jimenez ◽  
Nicolau Casal ◽  
Joel Gonzalez ◽  
Nuria Panella-Riera ◽  
...  
Keyword(s):  
Body Weight ◽  
Heat Stress ◽  
Social Interactions ◽  
Growing Pigs ◽  
Maximum Temperature ◽  
Lower Body Weight ◽  
Body Weights ◽  
Weight Gains ◽  
Feeding Area ◽  
Environmental Temperatures

Heat stress and competition for food are two major challenges in pigs reared in intensive conditions. The aim of the present work was to study the effect of providing a double feeder for pigs reared under two different environmental temperatures. In addition, two types of flooring, of 100% slat and 30% slat 70% concrete, were also considered. A total of 256 pigs in the growing-finishing period (from 27 kg to 110 kg) were housed using two environmental temperatures: control (from 18 °C to 25 °C) and heat stress (above 30 °C six hours a day). They were housed in 32 pens of 8 pigs each, distributed into 4 rooms (16 with one feeder and 16 with two). Pigs subjected to temperatures above 30 °C up to six hours had lower body weight gains than pigs subjected to a maximum temperature of 25 °C, confirming that thermal stress negatively affects performance in pigs. In addition, heat stress affected the final product by decreasing the lean percentage of carcasses by 2.6%. A double feeder reduced the presence of negative social behavior, especially in the feeding area, but body weight was lower than when one single feeder was used. A 30% slat 70% concrete floor showed better results in the pig stress indicators and body weights than 100% slat. It is concluded that providing a double feeder in the pens, although reducing the presence of negative social interactions, negatively affected body weight, in comparison to pigs fed with just one feeder.

Vasoactive intestinal peptide prevents PKCε-induced intestinal epithelial barrier disruption during EPEC infection

2015 ◽  
Vol 308 (5) ◽  
pp. G389-G402 ◽  
Author(s):  
V. Morampudi ◽  
V. S. Conlin ◽  
U. Dalwadi ◽  
X. Wu ◽  
K. C. Marshall ◽  
...  
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Critical Role ◽  
Term Treatment ◽  
Epithelial Barrier ◽  
Protective Effects ◽  
Short Term Treatment ◽  
Barrier Integrity ◽  
Barrier Disruption ◽  
Long Term Treatment

We previously showed that vasoactive intestinal peptide (VIP) protects against bacterial pathogen-induced epithelial barrier disruption and colitis, although the mechanisms remain poorly defined. The aim of the current study was to identify cellular pathways of VIP-mediated protection with use of pharmacological inhibitors during enteropathogenic Escherichia coli (EPEC) infection of Caco-2 cell monolayers and during Citrobacter rodentium-induced colitis. EPEC-induced epithelial barrier disruption involved the PKC pathway but was independent of functional cAMP, Rho, and NF-κB pathways. VIP mediated its protective effects by inhibiting EPEC-induced PKC activity and increasing expression of the junctional protein claudin-4. Short-term treatment with TPA, which is known to activate PKC, was inhibited by VIP pretreatment, while PKC degradation via long-term treatment with TPA mimicked the protective actions of VIP. Immunostaining for specific PKC isotypes showed upregulated expression of PKCθ and PKCε during EPEC infection. Treatment with specific inhibitors revealed a critical role for PKCε in EPEC-induced barrier disruption. Furthermore, activation of PKCε and loss of barrier integrity correlated with claudin-4 degradation. In contrast, inhibition of PKCε by VIP pretreatment or the PKCε inhibitor maintained membrane-bound claudin-4 levels, along with barrier function. Finally, in vivo treatment with the PKCε inhibitor protected mice from C. rodentium-induced colitis. In conclusion, EPEC infection increases intracellular PKCε levels, leading to decreased claudin-4 levels and compromising epithelial barrier integrity. VIP inhibits PKCε activation, thereby attenuating EPEC-induced barrier disruption.

scholarly journals Heat stress-induced renal damage in poultry and the protective effects of HSP60 and HSP47

2018 ◽  
Vol 23 (5) ◽  
pp. 1033-1040 ◽  
Author(s):  
Shu Tang ◽  
Shuang Zhou ◽  
Bin Yin ◽  
Jiao Xu ◽  
Liangjiao Di ◽  
...  
Keyword(s):  
Heat Stress ◽  
Renal Damage ◽  
Protective Effects

scholarly journals TrxR2 overexpression alleviates inflammation-mediated neuronal death via reducing the oxidative stress and activating the Akt–Parkin pathway

2019 ◽  
Vol 8 (5) ◽  
pp. 641-653 ◽  
Author(s):  
Jinbao Gao ◽  
Yunjun Li ◽  
Wende Li ◽  
Haijiang Wang
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Cell Viability ◽  
Western Blotting ◽  
Neuronal Death ◽  
Protective Effects ◽  
Mitochondrial Apoptosis ◽  
Inflammation Response ◽  
N2a Cells

Abstract Neuronal death caused by inflammatory cytokine-mediated neuroinflammation is being extensively explored. Thioredoxin reductase (TrxR) 2 is a novel mediator of inflammation response. In the current study, we focus on the mechanisms of TrxR2 overexpression in inflammation-mediated neuronal death. LPS was used to induce neuroinflammation in N2a cells in vitro. Adenovirus-loaded TrxR2 was transfected into N2a cells to up-regulate TrxR2 expression. Then, cell viability was determined via MTT assay and TUNEL assay. Apoptosis was measured via western blotting and ELISA. Oxidative stress was detected via ELISA and flow cytometry. A pathway inhibitor was used to verify the role of the Akt–Parkin pathway in the LPS-mediated N2a cell death in the presence of TrxR2 overexpression. With the help of immunofluorescence assay and western blotting, we found that TrxR2 expression was significantly reduced in response to LPS treatment, and this effect was associated with N2a cell death via apoptosis. At the molecular level, TrxR2 overexpression elevated the activity of the Akt–Parkin pathway, as evidenced by the increased expression of p-Akt and Parkin. Interestingly, inhibition of the Akt–Parkin pathway abolished the regulatory effect of TrxR2 on LPS-treated N2a cells, as evidenced by the decreased cell viability and increased apoptotic ratio. Besides, TrxR2 overexpression also reduced oxidative stress, inflammation factor transcription and mitochondrial apoptosis. However, inhibition of Akt–Parkin axis abrogated the protective effects of TrxR2 on redox balance, mitochondrial performance and cell survival. LPS-mediated neuronal death was linked to a drop in TrxR2 overexpression and the inactivation of the Akt–Parkin pathway. Overexpression of TrxR2 sustained mitochondrial function, inhibited oxidative stress, repressed inflammation response, and blocked mitochondrial apoptosis, finally sending a pro-survival signal for the N2a cells in the setting of LPS-mediated inflammation environment.

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