Chronic heat stress promotes liver inflammation in broilers via enhancing NF-κB and NLRP3 signaling pathway

Abstract Background The study was to investigate the effects of chronic heat stress on liver inflammatory injury and its potential mechanisms in broilers. Chickens were randomly assigned to 1-week control group (Control 1), 1-week heat stress group (HS1), 2-week control group (Control 2), and a 2-week heat stress group (HS2) with 15 replicates per group. Broilers in heat stress groups exposed to heat stress (35 ± 2°C) for 8 h/d with 7 or 14 consecutive days. Growth performance and liver inflammation injury were examined for the analysis of liver injury.ResultsThe results showed that heat stress decreased the growth performance, showed obvious blutpunkte, lowered liver weight and liver index, which resulted in significant liver damage of broilers. Both the gene and protein expressions of HSP70, TLR4 and NF-κB in the liver were significantly enhanced by heat stress. Furthermore, heat stress obviously enhanced IL-6, TNF-α, NF-κB P65, IκB and their phosphorylated proteins expressions in the liver of broilers. In addition, heat stress promoted the activation of NLRP3 with increased NLRP3, caspase-1 and IL-1β. ConclusionsThese results suggested that heat stress can cause the liver inflammation via activation of TLR4-NF-κB and NLRP3 signaling pathway in broilers.

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Effect of chitosan on blood profile, inflammatory cytokines by activating TLR4/NF-κB signaling pathway in intestine of heat stressed mice

Scientific Reports ◽

10.1038/s41598-021-98931-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Sahar Ghulam Mohyuddin ◽

Aftab Qamar ◽

Can-ying Hu ◽

Sheng-Wei Chen ◽

Jia-ying Wen ◽

...

Keyword(s):

Heat Stress ◽

Oral Administration ◽

Immune Function ◽

Control Group ◽

Mrna Levels ◽

Protective Effects ◽

Blood Profile ◽

Stress Group ◽

Tnf Α ◽

Body Heat

AbstractHeat stress can significantly affect the immune function of the animal body. Heat stress stimulates oxidative stress in intestinal tissue and suppresses the immune responses of mice. The protecting effects of chitosan on heat stress induced colitis have not been reported. Therefore, the aim of this study was to investigate the protective effects of chitosan on immune function in heat stressed mice. Mice were exposed to heat stress (40 °C per day for 4 h) for 14 consecutive days. The mice (C57BL/6J), were randomly divided into three groups including: control group, heat stress, Chitosan group (LD: group 300 mg/kg/day, MD: 600 mg/kg/day, HD: 1000 mg/kg/day). The results showed that tissue histology was improved in chitosan groups than heat stress group. The current study showed that the mice with oral administration of chitosan groups had improved body performance as compared with the heat stress group. The results also showed that in chitosan treated groups the production of HSP70, TLR4, p65, TNF-α, and IL-10 was suppressed on day 1, 7, and 14 as compared to the heat stress group. In addition Claudin-2, and Occludin mRNA levels were upregulated in mice receiving chitosan on day 1, 7, and 14 of heat stress. Furthermore, the IL-6, IL-10, and TNF-α plasma levels were down-regulated on day 1, 7, and 14 of heat stress in mice receiving the oral administration of chitosan. In conclusion, the results showed that chitosan has an anti-inflammatory ability to tolerate hot environmental conditions.

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Effects of Moringa Oleifera Leaf Polysaccharide on Growth Performance and Immune Response of Broiler Chickens

10.21203/rs.3.rs-1089038/v1 ◽

2021 ◽

Author(s):

Hosameldeen Mohamed Husien ◽

JunJie Huang ◽

WeiLong Peng ◽

ShuMei Zheng ◽

JinGui Li

Keyword(s):

Immune Response ◽

Growth Performance ◽

Broiler Chickens ◽

Moringa Oleifera ◽

The Body ◽

Feed Consumption ◽

Feed Additive ◽

Control Group ◽

High Dose ◽

Tnf Α

Abstract Moringa oleifera (MO) is a widely used as the nutritious and non-traditional feed supplementation containing kinds of bioactive substances. However, the enhancement effect of Moringa oleifera leaf Polysaccharide (MOLP) as a feed additive in broilers growth performance and immunity remains unclear. In this study, MOLP was obtained by water extraction and alcohol precipitation method, then purified with Trichloroacetic acid (TCA) assay. Chickens were randomly divided into 4 groups, to receive different doses of MOLP (0, 0.1, 0.2, 0.4g/kg) in feed for 3 weeks. The body weight gain (BWG) and feed consumption were recorded for feed conversion ratio (FCR) and average daily feed intake (ADFI) calculation. Broiler chickens were sacrificed and sampled on day 14, 21, 28 (D 14, D 21, and D 28) respectively. Serological indicators, including total protein (TP), albumin (ALB), globulin (GLO), and creatinine (CREA) were detected. ELISA kits were applied for detecting the levels of immunoglobulin A (IgA), immunoglobulin G (IgG), interleukin-2 (IL-2), and tumor necrosis factor (TNF-α). From D 21 to D 28, the results showed that middle dose of MOLP significantly increased BWG and ADFI as well as liver and bursa indexes when compared with the control group. In addition, TP and GLO were also increased (P<0.05). All MOLP treatments enhanced the serum concentrations of IgG and IL-2 (P<0.01). Furthermore, results of quantitative RT-PCR showed that high dose of MOLP treatment significantly increased (P<0.001) the mRNA expression levels of IL-2 and TNF-α of chickens relative to the control group. In conclusion, the results showed that MOLP supplementation contributed to improve growth performance and immune response in broiler chickens, and MOLP could be considered as a promising feed additive.

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Comparative Transcriptome Analysis Reveals the Protective Mechanism of Glycyrrhinic Acid for Deoxynivalenol-Induced Inflammation and Apoptosis in IPEC-J2 Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/5974157 ◽

2020 ◽

Vol 2020 ◽

pp. 1-17

Author(s):

Xiaoxiang Xu ◽

Guorong Yan ◽

Juan Chang ◽

Ping Wang ◽

Qingqiang Yin ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Transcriptome Analysis ◽

Animal Feed ◽

Control Group ◽

Protective Mechanism ◽

Dependent Manner ◽

Gene Expressions ◽

Lactate Dehydrogenase Release ◽

Tnf Α

Deoxynivalenol (DON) is the most common mycotoxin that frequently contaminates human food and animal feed, resulting in intestinal diseases and systemic immunosuppression. Glycyrrhinic acid (GA) exhibits various pharmacological activities. To investigate the protective mechanism of GA for DON-induced inflammation and apoptosis in IPEC-J2 cells, RNA-seq analysis was used in the current study. The IPEC-J2 cells were treated with the control group (CON), 0.5 μg/mL DON, 400 μg/mL GA, and 400 μg/mL GA+0.5 μg/mL DON (GAD) for 6 h. Results showed that 0.5 μg/mL DON exposure for 6 h could induce oxidative stress, inflammation, and apoptosis in IPEC-J2 cells. GA addition could specifically promote the proliferation of DON-induced IPEC-J2 cells in a dose- and time-dependent manner. In addition, GA addition significantly increased Bcl-2 gene expression ( P < 0.05 ) and superoxide dismutase and catalase activities ( P < 0.01 ) and decreased lactate dehydrogenase release, the contents of malonaldehyde, IL-8, and NF-κB ( P < 0.05 ), the relative mRNA abundances of IL-6, IL-8, TNF-α, COX-2, NF-κB, Bax, and caspase 3 ( P < 0.01 ), and the protein expressions of Bax and TNF-α. Moreover, a total of 1576, 289, 1398, and 154 differentially expressed genes were identified in CON vs. DON, CON vs. GA, CON vs. GAD, and DON vs. GAD, respectively. Transcriptome analysis revealed that MAPK, TNF, and NF-κB signaling pathways and some chemokines played significant roles in the regulation of inflammation and apoptosis induced by DON. GA may alleviate DON cytotoxicity via the TNF signaling pathway by downregulating IL-15, CCL5, and other gene expressions. These results indicated that GA could alleviate DON-induced oxidative stress, inflammation, and apoptosis via the TNF signaling pathway in IPEC-J2 cells.

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Chronic heat stress regulates the relation between heat shock protein and immunity in broiler small intestine

Scientific Reports ◽

10.1038/s41598-020-75885-x ◽

2020 ◽

Vol 10 (1) ◽

Cited By ~ 1

Author(s):

Sharif Hasan Siddiqui ◽

Darae Kang ◽

Jinryong Park ◽

Mousumee Khan ◽

Kwanseob Shim

Keyword(s):

Body Weight ◽

Small Intestine ◽

Heat Stress ◽

Treatment Group ◽

Heat Shock ◽

Heat Shock Protein ◽

Growth Performance ◽

Control Group ◽

Immune Functions ◽

Negative Effect

Abstract Chronic heat stress is considered to decrease the immune functions which makes negative effect on broiler growth performance. Here, we investigated the relationship between chronic heat stress, growth performance, and immunity in the small intestine of broilers. The study included two groups (control and heat stressed group) with eight replications per group. Ten broilers of 20-day aged were allocated in each replication. On day 35, the treatment group was subdivided into two groups based on their body weights (heavy and low body weight). Although, there was only the control and treatment group on day 28. The growth performance decreased and expression of heat shock protein 70 (HSP70), HSP60, and HSP47 increased on days 28 and 35 in the chronic heat stress group as compared with those in the control group. The expression levels of HSPs were significantly higher in the low body weight group than in the control group. The genes HSP70 and HSP60 were significantly associated with pro- and anti-inflammatory cytokines in the small intestine of the broilers of the treatment group. Thus, HSP70 and HSP60 activated the adaptive immunity in the small intestines of the broilers from the treatment group to allow adaptation to chronic heat stress environment.

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Heat stress combined with lipopolysaccharide alter the activity and superficial molecules of peripheral monocytes

International Journal of Immunopathology and Pharmacology ◽

10.1177/2058738419828891 ◽

2019 ◽

Vol 33 ◽

pp. 205873841982889

Author(s):

Jiajing Luo ◽

Yi Chen ◽

Chengjia Ding ◽

Jialing Qiu ◽

Yulan Chen ◽

...

Keyword(s):

Flow Cytometry ◽

Heat Stress ◽

Western Blot ◽

Inflammatory Mediators ◽

Peripheral Blood ◽

Heat Stroke ◽

Enzyme Linked Immunosorbent Assay ◽

Control Group ◽

Rt Pcr ◽

Tnf Α

The purpose of this study was to focus on the underlying relationship between the hyperactivity for the peripheral monocytes and heat stroke by investigating the inflammatory oxidative activity of and the expression of superficial molecules. Peripheral blood samples were collected from 10 healthy adult volunteers. Human blood monocytes were isolated by density gradient centrifugation and sequent adherent culture. The objectives were divided into four groups: 43°C heat stress combined with lipopolysaccharide (LPS) group, 43°C heat stress group, LPS group, and control group. There were 10 cases in each group. An enzyme-linked immunosorbent assay (ELISA) test was used to measure the concentrations of supernatant inflammatory mediators (tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10)). After loaded by 2,7-Dichlorodi-hydrofluorescein-diacetate (DCFHDA) fluorescent probe, intracellular reactive oxygen species (ROS) levels were determined by a flow cytometry. After fluorescent microspheres incubation, the phagocytosis of monocytes was observed under a fluorescent microscope. Respectively, the flow cytometry and Western blot were used to evaluate the level of triggering receptor expressed on myeloid cells-1 (TREM-1) and Toll-like receptor-4 (TLR-4) on the monocytes. Furthermore, the mRNA expression of TREM-1 and TLR-4 was detected by real-time polymerase chain reaction (RT-PCR). The heat stress combined with LPS stimulation promoted the peripheral monocytes to produce inflammatory mediators (TNF-α, IL-1β, and IL-10) and release ROS. Otherwise, such complex strike significantly suppressed the phagocytic activity of monocytes in peripheral blood. Moreover, the expression of TREM-1, TLR-4 and CD86 was measured by the flow cytometry on peripheral monocytes which were respectively promoted by the union of heat stress and LPS. The results of Western blot and RT-PCR demonstrated the similar kinetics on these superficial molecules (TREM-1, TLR-4, and CD86) stimulated by the combination of heat stress and LPS. The underlying mechanism of the dysfunction for the peripheral monocytes may be related to the abnormal expression of superficial molecules TREM-1, TLR-4, and CD86 on the monocytes induced by heat stress and LPS.

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The effect of low-intensity resistance training after heat stress on muscle size and strength of triceps brachii: a randomized controlled trial

BMC Musculoskeletal Disorders ◽

10.1186/s12891-019-2991-4 ◽

2019 ◽

Vol 20 (1) ◽

Cited By ~ 2

Author(s):

Masatoshi Nakamura ◽

Tomoichi Yoshida ◽

Ryosuke Kiyono ◽

Shigeru Sato ◽

Nobushige Takahashi

Keyword(s):

Heat Stress ◽

Resistance Training ◽

Muscle Strength ◽

Muscle Thickness ◽

Control Group ◽

Triceps Brachii ◽

Stress Group ◽

Repetition Maximum ◽

Low Intensity ◽

The One

Abstract Background The purpose of this study was to clarify whether there is a synergistic effect on muscular strength and hypertrophy when low-intensity resistance training is performed after heat stress. Methods Thirty healthy young male volunteers were randomly allocated to either the low-intensity resistance training with heat stress group or the control group. The control group performed low-intensity resistance training alone. In the low-intensity resistance training with heat stress group, a hot pack was applied to cover the muscle belly of the triceps brachii for 20 min before the training. The duration of the intervention was 6 weeks. In both groups, the training resistance was 30% of the one repetition maximum, applied in three sets with eight repetitions each and 60-s intervals. The one repetition maximum of elbow extension and muscle thickness of triceps brachii were measured before and after 6 weeks of low intensity resistance training. Results There was no significant change in the one-repetition maximum and muscle thickness in the control group, whereas there was a significant increase in the muscle strength and thickness in the low-intensity resistance training with heat stress group. Conclusion The combination of heat stress and low-intensity resistance training was an effective method for increasing muscle strength and volume. Trial registration University Hospital Medical Information Network Clinical Trials Registry (UMIN000036167; March 11, 2019).

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Protective effects of ginkgolide on a cellular model of Alzheimer’s disease via suppression of the NF-κB signaling pathway

10.21203/rs.3.rs-791848/v1 ◽

2021 ◽

Author(s):

Tiantong Niu ◽

He Yin ◽

Baolei Xu ◽

Tingting Yang ◽

Huiqin Li ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Cell Viability ◽

Mrna Expression ◽

Signaling Pathway ◽

Hek293 Cells ◽

Control Group ◽

Cellular Model ◽

Intracellular Protein ◽

Tnf Α

Abstract NF-κB signaling has been reported to play a key regulatory role in the pathogenesis of Alzheimer’s disease (AD). The purpose of this study is to investigate the effects of ginkgolide on cell viability in an AD cellular model involving an APP/PS1 double gene-transfected HEK293 cell line (APP/PS1-HEK293) and further explored the mechanisms of action related to NF-κB signaling. The optimal time point and concentration of ginkgolide for cell proliferation were screened using a cell counting kit-8 assay. Based on the results, an in vitro study was performed by co-culture of APP/PS1-HEK293 with different dosages of ginkgolide, followed by an enzyme-linked immunosorbent assay to measure the levels of supernatant tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, as well as western blotting and real-time polymerase chain reaction to detect intracellular protein and mRNA expression of NF-κB p65, IκBa, Bcl-2 and Bax. APP/PS1-HEK293 cells exhibited the highest cell viability at a concentration of 100 µg/ml after 48 h of treatment with ginkgolide. The supernatant levels of TNF-α, IL-1β and IL-6 in the high-dosage ginkgolide-treated groups were lower than those in the control group. Compared with the control group, there were decreased intracellular protein and mRNA expression of NF-κB p65 and Bax, but increased protein and mRNA expression of IκBa in both high-dosage and low-dosage group. Ginkgolide may enhance cell viability, indicative of its neuroprotective effects on AD, at least partially via suppression of the NF-κB signaling pathway involving anti-apoptosis and anti-inflammation mechanisms. Therefore, ginkgolide might be a promising therapeutic agent against AD.

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Octreotide ameliorates hypoxia/reoxygenation-induced cerebral infarction by inhibiting oxidative stress, inflammation and apoptosis, and via inhibition of TLR4/MyD88/NF-κB signaling pathway

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v20i11.4 ◽

2021 ◽

Vol 20 (11) ◽

pp. 2261-2266

Author(s):

Yanbin Hou ◽

Zhongze Lou ◽

Yunxin Ji ◽

Liemin Ruan ◽

He Gao

Keyword(s):

Oxidative Stress ◽

Cerebral Infarction ◽

Signaling Pathway ◽

Control Group ◽

N2a Cells ◽

Tnf Α ◽

Octreotide Treatment ◽

Vitro Model ◽

Hypoxia Reoxygenation

Purpose: To explore the effects of octreotide (OCT) on oxidative stress, inflammation and apoptosis in hypoxia/reoxygenation (H/R)-induced cerebral infarction.Methods: The in vitro model of cerebral infarction was established by treating N2A cells with hypoxia for 4 h and reoxygenation for 24 h. The viability of N2A cells was determined by CCK-8 assay. The cells were divided into 3 groups: control group, H/R group, and H/R+OCT group. The cells in H/R+OCT group were pretreated with OCT (60 ng/mL) before H/R treatment. The oxidative stress of N2A cells were assessed by determining the levels of superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT), reactive oxygen species (ROS) and malondialdehyde (MDA). Inflammation of N2A cells was evaluated by evaluating the levels of TNF-α, IL-1β, IL-6, and IL-8, while the apoptosis of N2A cells was assessed by flow cytometry. Western blot analysis was used to determine the expression of Bcl-2, Bax, TLR4, MyD88, and NF-κB.Results: Octreotide treatment significantly reduced the level of oxidative stress. The inflammation of N2A cells caused by hypoxia/reoxygenation was inhibited by treatment with octreotide. Apoptosis of N2A cells was also inhibited by octreotide treatment. Hypoxia/reoxygenation activated TLR4/MyD88/NF-κB signaling pathway, while octreotide inhibits the activation of this pathway.Conclusion: The results reveal that octreotide inhibits hypoxia/reoxygenation-induced oxidative stress,as well as the inflammation, and apoptosis of N2A cells by inhibiting TLR4/MyD88/NF-κB signaling pathway. Thus, these findings may provide new insights into the treatment of cerebral infarction.

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Dietary seaweed-derived polysaccharides improve growth performance of weaned pigs through maintaining intestinal barrier function and modulating gut microbial populations

10.21203/rs.3.rs-64432/v2 ◽

2020 ◽

Author(s):

Tiande Zou ◽

Jin Yang ◽

Xiaobo Guo ◽

Qin He ◽

Zirui Wang ◽

...

Keyword(s):

Growth Performance ◽

Intestinal Barrier ◽

Basal Diet ◽

Intestinal Barrier Function ◽

Control Group ◽

Mrna Levels ◽

Intestinal Health ◽

Weaned Pigs ◽

Tnf Α ◽

G Ratio

Abstract Background: Seaweed-derived polysaccharides (SDP) represent an attractive source of prebiotic nutraceuticals for the food and animal husbandry industry. However, the mechanism by which SDP from Enteromorpha mediates pig growth are not fully understood. This study aimed to investigate how SDP supplementation influences the growth performance and intestinal health in weaned pigs.Results: In Exp. 1, 240 weaned pigs were randomly assigned to four dietary treatments and fed with a basal diet or a basal diet containing 200, 400 or 800 mg/kg SDP, respectively, in a 21-d trial. Pigs on the 400 or 800 mg/kg SDP-supplemented group had greater ADG and lower F/G ratio than those on the control group (P＜0.05). In Exp. 2, 20 male weaned pigs were randomly assigned to two treatments and fed with a basal diet (CON group) or a basal diet supplemented with 400 mg/kg SDP (the optimum does from Exp. 1), in a 21-d trial. Pigs fed the SDP diet had greater ADG, the concentrations of serum IL-6 and TNF-α and the activities of glutathione peroxidase, superoxide dismutase and catalase (P＜0.05), and lower F/G, diarrhea rate, as well as serum D-lactate concentrations and diamine oxidase activity (P＜0.05). Moreover, dietary SDP supplementation enhanced secretory immunoglobulin A content, villus height and villous height: crypt depth ratio in small intestine, as well as the lactase and maltase activities in jejunum mucosa (P＜0.05). SDP supplementation elevated the mRNA levels of inflammatory response-related genes (IL-6, TNF-α, TLR4, TLR6 and MyD88), and the mRNA and protein levels of ZO-1, Claudin-1 and Occludin in jejunum mucosa (P＜0.05). Importantly, SDP not only increased the Lactobacillus population but also reduced the Escherichia coli population in cecum (P＜0.05). Furthermore, SDP increased acetic acid and butyric acid concentrations in cecum (P＜0.05).Conclusions: These results not only suggest a beneficial effect of SDP on growth performance and intestinal barrier functions, but also offer potential mechanisms behind SDP-facilitated intestinal health in weaned pigs.

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Hyperthermia Affects Immune and Oxidative Stress Indices of Immune Organs of Broilers by Changing the Expressions of ABCG2, SVCT-2 and MCU

10.21203/rs.3.rs-936596/v1 ◽

2021 ◽

Author(s):

Xiuheng Xue ◽

Chunhuan Ren ◽

Luping Wang ◽

Mengzhu Xu Xu ◽

Caiyun Fan ◽

...

Keyword(s):

Oxidative Stress ◽

Heat Stress ◽

Immune Function ◽

Immunoglobulin M ◽

Control Group ◽

Rt Pcr ◽

Stress Group ◽

Immune Organs ◽

Significant Difference ◽

And Oxidative Stress

Abstract Background: As global temperatures rise, heat stress has become one of the major environmental stressors in the poultry industry. The purpose of the study was to investigate the effects of heat stress on immune function and oxidative stress, and further reveal the possible mechanisms of oxidative stress induced by heat stress for thymus and spleen of broilers. Methods: At the age of 28 days, thirty broilers were randomly divided into the control group (25 ± 2°C; 24 h/day) and the heat stress group (36 ± 2°C; 8 h/day); the experience was lasted for 1 week. At the end of the experience, the broilers per group were respectively euthanized and collected some samples, then to be analyzed. Results: The results showed that the levels of heat shock proteins 70 (HSP70,P＜ 0.01), corticosterone (CORT,P＜ 0.01), the contents of malondialdehyde (MDA, P＜ 0.05), interleukin-6 (IL-6, P＜ 0.01) and tumor necrosis factor-alpha (TNF-α, P＜ 0.01) in serum were significantly higher in heat stress group than that in the control group; The activities of total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) and contents of glutathione (GSH) in heat stress group significantly reduced (P＜ 0.05) in serum. Compared with the control group, the birds subjected to heat stress reduced the weight (P＜ 0.01) and the indices of thymus (P＜ 0.01), the activities of T-AOC (P＜ 0.01) and SOD (P＜ 0.05) of spleen, and levels of IL-10 (P＜ 0.05) and the GSH-PX (P＜ 0.05) in thymus and spleen, and increased the IL-6 content of thymus (P＜ 0.05), the MDA content (P＜ 0.01), and the reactive oxygen species (ROS) levels (P＜ 0.01) in thymus and spleen. Moreover, the expression of immunoglobulin G (IgG) gene in thymus and spleen of heat stressed broiler significantly increased by reverse transcription-polymerase chain reaction (RT-PCR) and real time RT-PCR (qRT-PCR; P＜ 0.05); However, the expression of immunoglobulin M (IgM) gene in spleen significantly increased (P＜ 0.05), and had no significant difference (P＞ 0.05) in thymus of heat-stressed broiler. Furthermore, the relative expression of ATP binding cassette subfamily G member 2 (ABCG2) in thymus and spleen (P＜ 0.05), sodium dependent vitamin C transporter-2 (SVCT-2, P＜ 0.01) and mitochondria calcium uniporter (MCU, P＜ 0.01) mRNA in thymus of heat stressed broilers significantly increased; and the expression of ABCG2 (P＜ 0.05), SVCT-2 (P＜ 0.01) and MCU (P＜ 0.01) protein of thymus and spleen in the heat-stressed broiler increased significantly compared with the control group. Conclusions: In summary, the study confirmed that heat stress caused oxidative stress to immune organs of broilers, further reduced immune function. Moreover, the potential mechanisms of heat stress-induced oxidative stress for thymus and spleen was further reveal in broilers.

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