Intestinal inflammation poses a significant challenge to pig production, as it impairs gut health, compromises growth performance, and results in substantial economic losses. Therefore, preventing and controlling intestinal inflammation in pigs is essential for maintaining intestinal health and production efficiency. Short-chain fatty acids (SCFAs) are gut microbiota metabolites that play an important role in alleviating intestinal inflammation by regulating macrophage function. Mechanistic insights largely derived from murine and in vitro studies have revealed that SCFAs regulate macrophage mediated inflammation through mechanisms involving histone deacetylases (HDACs), nuclear factor-κB (NF-κB), and other pathways. Moreover, nutritional strategies such as dietary fiber, prebiotics, and fermented feed for alleviating intestinal inflammation in pigs are discussed. This review aims to provide a theoretical foundation for developing SCFA-based nutritional interventions to improve gut health, immune regulation, and production performance in pigs.

Myokines are defined as a class of bioactive molecules-including metabolites, peptides, and proteins-released from skeletal muscle cells and promoted by exercise. Recently, myokine-mediated muscle-organ crosstalk has sparked increased interest. Skeletal muscle secretes hundreds of myokines in an autocrine, paracrine, or endocrine manner, mediating the crosstalk between skeletal muscle and skeletal muscle itself, bone, fat, liver, and so on to regulate the physiological state of multiple organs, exerting a wide range of benefits of exercise. The relationship between muscle and myokines may be better understood as an exercise-responsive regulatory framework involving skeletal muscle and myokines, although direct evidence for an integrated bidirectional feedback network remains incomplete. In the network, myokines regulate skeletal muscle metabolism and remodeling through autocrine/paracrine actions, while exercise-induced muscle-derived signals may also contribute to long-lasting systemic adaptations involving immune mobilization, redox homeostasis, gut microbiota-related metabolic remodeling, and gut-muscle-bone crosstalk. Therefore, the distinct feature of skeletal muscle is not the mere presence of bidirectional signaling but its large mass, fiber-type metabolic heterogeneity, and direct responsiveness to repeated mechanical stimuli during exercise. On the one hand, as a source of myokines, the stimulation of skeletal muscle affects the production of myokines through various signaling pathways. On the other hand, myokines affect skeletal muscle function, such as glucose absorption, fatty acid oxidation, skeletal muscle mass, and muscle fiber type transformation. What's more, some myokines are muscle fiber type-specific, meaning that the expression of myokines may be influenced by muscle fiber type. Based on these, this review aims to summarize current evidence for exercise-responsive interactions between skeletal muscle and myokines and to identify where feedback regulation remains hypothetical.

This study evaluated the effects of dietary distillers' dried grains with solubles (DDGS) levels on nutrient digestibility, meat quality, and intestinal health in meat ducks. In a 28-d feeding trial (Exp. 1), 400 Cherry Valley ducks (average body weight [BW] = 658.73 ± 3.79 g, age = 14 d old) were randomly assigned to five groups receiving 0 (CON), 5%, 10%, 15%, or 20% DDGS. Each treatment had eight replicates (cages) with ten ducks per replicate. A subsequent metabolism trial (Exp. 2) was conducted using the same diets. At 42 d of age, two ducks per replicate were randomly selected and fed diets supplemented with 0.5% titanium dioxide for digestibility determination. Results showed that 20% DDGS significantly reduced the digestibility of gross energy (GE; P = 0.010) and crude protein (CP; P = 0.026) compared to the CON group. As DDGS increased, CP digestibility decreased linearly (P = 0.001) and quadratically (P = 0.049). Serum triglyceride levels were significantly increased in the 20% DDGS group (P = 0.034). For meat quality, DDGS decreased breast muscle lightness (L∗45 min, P = 0.031) and increased yellowness (b∗45 min, P = 0.028). Shear force of breast muscle increased significantly in the 20% DDGS group (P = 0.009) and increased linearly with DDGS (P = 0.015). Histologically, DDGS supplementation decreased muscle fiber density (P = 0.005) and jejunal villus height (P = 0.001), but increased muscle fiber diameter (P = 0.027). Both muscle fiber diameter and density showed significant linear relationships with increasing DDGS levels (P = 0.003 and P < 0.001, respectively). Cecal butyric acid level decreased at 15% and 20% inclusion (P < 0.05), and valeric acid level decreased at 20% inclusion (P < 0.001). Notably, 10% DDGS increased cecal microbial diversity and the abundance of beneficial Prevotellaceae (P < 0.05). In summary, dietary inclusion of 5%-20% DDGS did not adversely affect growth performance, carcass traits, and organ indices in ducks. While higher levels impaired some meat quality traits, 10% DDGS was identified as the optimal level, improving intestinal microbiota without compromising overall production performance. These findings support the partial replacement of corn-soybean meal with DDGS in duck diets.

This study aimed to explore the alleviating effect of different levels of dietary stevia extract on mice challenged with lipopolysaccharide (LPS) and the possible mechanisms were explored. In this experiment, ninety 3-week-old healthy male Kunming mice with comparable body weights were randomly allocated into five groups, namely the control group, LPS group, and LPS + stevia extract groups at doses of 200, 400 and 600 mg/kg, respectively. Each group comprised 18 mice, with 6 replicates per treatment and 3 mice per replicate. The total feeding period was 28 days. On day 14 and day 28, at 9:00 a.m., the mice were intraperitoneally injected with 1 mg/mL LPS at a dosage of 3 mg/kg body weight (BW), whereas the control group was administered an equivalent volume of normal saline. Six hours post-injection on day 28, the body weights of the mice were recorded, and blood samples, liver tissues, and spleen tissues were collected sequentially. In this study, we found that LPS caused oxidative damage in the mouse spleen, led to splenic congestion, increased spleen index, lymphocyte infiltration and pathological lesions. Meanwhile, antioxidant capacity was compromised, as indicated by a decreasing (P < 0.05) in Glutathione peroxidase (GSH-Px) activity and increases (P < 0.05) in malondialdehyde (MDA) content in plasma and spleen. LPS also induced inflammatory response and increased (P < 0.05) levels of pro-inflammatory cytokines Tumor necrosis factor-alpha (TNF-α), Interleukin-1 beta (IL-1β), and Interleukin-6 (IL-6) in spleen. Furthermore, the expression of key proteins involved in Toll-like receptor 4 (TLR4)-initiated signaling pathway, including TLR4, Myeloid differentiation primary response 88 (MYD88), and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were increased (P < 0.05). Dietary supplementation with Stevia rebaudiana extract significantly reduced these LPS-induced effects, partially restored splenic tissue damage, and provided a protective effect by inhibiting the TLR4/MYD88/NF-κB signaling pathway through decreasing the expression of key nodal proteins like TLR4, MYD88, and NF-κB.

Pterostilbene (PTS), a more bioavailable analog of resveratrol (RES), is a promising natural metabolic regulator for improving metabolic health. The metabolic regulatory benefits of RES are believed to be associated with SIRT1 activation. However, the direct activation of SIRT1 by RES was proven to be an in vitro artifact. Here, we demonstrate that PTS is a more potent metabolic regulator than RES. More significantly, we have identified estrogen receptor α (ERα) as the intermediate signaling mediating SIRT1 expression by both RES and PTS. First, RES and PTS function as ERα agonists to stimulate Sirt1 transcription. Second, RES and PTS act as stabilizers of ERα-SIRT1 interaction, blocking ubiquitination and thereby enhancing their protein stability. Third, RES and PTS promote ERα deacetylation, subsequently increasing ERα transactivation. Finally, skeletal muscle-specific ERα knockout attenuates the metabolic regulatory benefits of PTS. Together, our study demonstrates that PTS is a more potent metabolic regulator than RES by activating the ERα/SIRT1 signaling.

Resveratrol is known to improve pork quality, and pterostilbene, a more bioavailable analog, may exert superior effects. This study aimed to compare the effects of dietary resveratrol and pterostilbene on pork quality and investigate their regulatory mechanisms. Fifty-four barrows (approximately 57 kg body weight), with three pigs per pen, were assigned to three groups: a control group fed a basal diet, and two treatment groups receiving the basal diet supplemented with 200 mg/kg resveratrol or pterostilbene. It was shown that neither resveratrol nor pterostilbene affected growth performance or carcass traits (P > 0.05). Furthermore, pterostilbene increased the redness of pork (P < 0.05), whereas resveratrol did not exhibit this effect (P > 0.05). Mechanistically, pterostilbene promoted myoglobin expression and modulated its redox status (P < 0.05), whereas resveratrol showed no such effects (P > 0.05). Furthermore, both resveratrol and pterostilbene enhanced muscle antioxidant capacity via Nrf2/Keap1 activation and promoted a fast-to-slow muscle fiber transition (P < 0.05), with pterostilbene exhibiting stronger effects (P < 0.05). The study highlights that, using the same supplementation, pterostilbene as a more effective feed additive than resveratrol for improving pork redness and expands the mechanistic understanding of stilbene-mediated regulation of meat color.

This study aimed to investigate the effects of stevia extract (SE) on growth performance and meat quality of broilers and reveal possibly mechanisms. Four hundred Arbor Acres male broilers (1 d old, 40 ± 1 g) were randomly assigned to 5 treatments with 8 replicates of 10 broilers per replicate. Broilers in the control (CON) group were fed the basal diet, while broilers in the other 4 treatment groups were fed the basal diet supplemented with 50, 100, 150, and 200 mg/kg SE, respectively. Dietary supplementation with SE effectively improved breast meat quality and tended to increase average daily gain (ADG) in broilers. Compared with the CON group, 150 mg/kg SE reduced 48 h drip loss and peak shear force of breast muscle (P < 0.05). Both 150 and 200 mg/kg SE decreased total cholesterol (TC) and triglyceride (TG) contents, while 100 and 150 mg/kg SE reduced malondialdehyde (MDA) concentration in breast muscle (P < 0.05). SE altered fatty acid (FA) composition: 150 mg/kg SE decreased the proportion of C24:0, and 200 mg/kg SE decreased C22:6n3 (P < 0.05). Linear regression analysis identified 150 mg/kg as the optimal SE level for meat quality improvement, which also downregulated FASN and ACACA mRNA expression (P < 0.05). Untargeted metabolomics revealed that 150 mg/kg SE modulated glycerophospholipid metabolism. Further validation confirmed that 150 mg/kg SE increased phospholipid (PL) content in breast muscle and improved endoplasmic reticulum (ER) and mitochondrial (MT) homeostasis. These changes were accompanied by reduced mRNA and protein expression of ER stress biomarkers (GRP78, PERK, IRE1, XBP1) and the MT chaperone HSP60 (P < 0.05). In conclusion, SE improves broiler breast meat quality via regulating the glycerophospholipid metabolism and enhancing endoplasmic reticulum and mitochondrial homeostasis. Regression analysis in this study indicates that the optimal SE supplementation amount for broilers is 150 mg/kg.

Oxidative stress impairs intestinal health in animals. As a potential antioxidant, l-theanine exerts anti-inflammatory and antioxidant effects. However, its biological functions and underlying mechanisms in intestinal oxidative damage remain unclear. This study aimed to investigate the protective effect of l-theanine against diquat-induced intestinal oxidative damage in mice and explore its potential molecular mechanisms. The results showed that dietary l-theanine supplementation significantly enhanced intestinal antioxidant capacity (reducing the levels of reactive oxygen species, malondialdehyde and hydrogen peroxide and elevating the activities of antioxidant enzymes), alleviated inflammation (downregulating pro-inflammatory cytokine levels and upregulating interleukin-10 mRNA expression), improved intestinal integrity (enhancing morphology, reducing permeability and upregulating tight junction-related genes), and boosted mitochondrial function (increasing mitochondrial membrane potential, adenosine triphosphate content and mitochondrial function-related gene expression) in oxidatively stressed mice. Concomitantly, l-theanine attenuated intestinal iron overload (inhibiting Fe2+ accumulation and upregulated ferritin heavy chain 1 expression) and suppressed the ferroptosis pathway (upregulating nuclear factor erythroid 2-related factor 2 (Nrf2), glutathione peroxidase 4 (GPX4), and solute carrier family 7 member 11 expression). In conclusion, l-theanine alleviates intestinal oxidative damage in oxidatively stressed mice by enhancing intestinal antioxidant capacity and inhibiting ferroptosis, a protective effect that may be mediated by the activation of the Nrf2/GPX4 signaling pathway.

Abstract Background The fact that feeding pigs with probiotic-fermented agricultural by-products improves pork quality has been repeatedly demonstrated and widely applied, but the underlying mechanisms remain unclear. This study explored the effects of fermented extruded brewers’ spent grain (FEBSG) on meat quality in growing-finishing pigs, as well as its regulatory mechanisms. Methods Sixty Duroc × Landrace × Yorkshire pigs (52.25 ± 2.10 kg) were randomly assigned to five dietary treatments, in which FEBSG replaced 0, 5%, 10%, 15%, and 20% of soybean meal (SBM). The experiment spanned 10 weeks. Results Compared with the control, 20% FEBSG significantly increased final body weight, average daily feed intake, and average daily gain, while decreasing feed to gain ratio (P < 0.05). Both 15% and 20% FEBSG improved carcass characteristics and meat quality, including higher carcass weight, loin eye area, and intramuscular fat content, along with lower drip loss and shear force (P < 0.05). These treatments also enhanced flavor-related amino acids and unsaturated fatty acids (P < 0.05), and improved umami and sweet taste profiles. Moreover, 20% FEBSG increased muscle fiber density and reduced fiber diameter, upregulated MyHC I, MyHC IIa, PGC-1α, AMPKα1, TFAM, and SDH activity, and downregulated MyHC IIb and LDH activity (P < 0.05). Proteomic analysis identified 69 differentially expressed proteins, with enrichment in AMPK and PPAR signaling pathways. Metagenomic analysis revealed increased abundance of short-chain fatty acid-producing bacteria, including Clostridium, Lactobacillus, Prevotella, and Bartonella. Correlation analysis demonstrated associations between gut microbiota diversity and meat quality traits, as well as between dominant microbial genera and differentially expressed proteins, volatile fatty acids, muscle fiber characteristics, and the AMPK/PGC-1α/TFAM signaling pathway. Conclusions Partial replacement of SBM with FEBSG positively influenced growth performance and pork quality in pigs, with the underlying mechanisms may involve the activation of the AMPK/PGC-1α/TFAM signaling pathway via the gut-muscle axis, thereby enhancing mitochondrial biogenesis, muscle development, and metabolism.

Eugenol (4-allyl-2-methoxyphenol), a natural phytogenic compound, exhibits physiological properties including antibacterial, anti-inflammatory, and antioxidant activities. This study aimed to evaluate the effects of dietary eugenol supplementation on lipid metabolism, carcass characteristics, and mechanism in finishing pigs. In our findings, dietary supplementation with eugenol significantly improved carcass traits in finishing pigs (P<.05). The eugenol-supplemented diet markedly reduced serum concentrations of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein (LDL) (P<.05), while significantly increasing high-density lipoprotein (HDL) levels (P<.05). Furthermore, eugenol supplemented diet significantly decreased the content of TC and TG in muscle tissue (P<.05). Specifically, EUG significantly downregulated the protein expression of acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and sterol regulatory element-binding protein (SREBP) in adipose tissue (P<.05). EUG treatment upregulated protein expressions of transient receptor potential vanilloid-1 (TRPV1) and P-AMPK/AMPK (P<.05). These results demonstrated that eugenol regulates lipid metabolism through the TRPV1/AMPK signaling pathway, effectively reducing serum TG and cholesterol levels while inhibiting lipid accumulation.

Water-holding capacity (WHC) is essential for both pork quality and industrial economics. Preliminary studies have shown that grape seed proanthocyanidin extract (GSPE) helps reduce drip loss in the longissimus thoracis (LT) muscle of finishing pigs. However, the mechanism by which GSPE affects the WHC of pork remains unclear. This study investigated the improvement in WHC of pork following dietary supplementation with GSPE. The research findings showed that adding GSPE to the diet significantly reduced drip loss, increased the proportion of bound water in the muscle, and improved muscle fiber rupture and separation. GSPE also significantly increased muscle pH value, reduced glycolytic potential, enhanced the expression of calpain-1 and integrin β1, and altered muscle fiber characteristics. In summary, the impact of GSPE on the WHC of LT muscle may be closely linked to the expression of cytoskeletal proteins, calpains, muscle fiber characteristics, and enzymes involved in the glycolysis pathway.

Low-intensity pulsed ultrasound stimulation (LIPUS) as a non-invasive, high-spatial resolution and high penetration depth brain modulation technology has been used for modulating neuromuscular function. However, the modulation of neural electrical signal changes in the neuromuscular system by LIPUS remains to be explored. In this study, we stimulated the mouse brain motor cortex by LIPUS with different number of tone burst (NTB) and recorded the local field potential (LFP) signals of the target region and electromyography (EMG) of tail muscle. Multi-Scale Transfer Entropy (MSTE) analysis method was used to explore the multi-scale synchronization characteristics and functional cortico-muscular coupling (FCMC) strength changes of mice LFP-EMG before and after LIPUS under different NTBs. The results show that the MSTE of LFP-EMG before and after LIPUS stimulation was higher than that of EMG-LFP. After adding multi-scale, MSTE has a significant relationship with time scales. When NTB = 200, the scale of extremum is the largest. There was a fitting intersection between LFP-EMG and EMG-LFP scale 7-21 before and after stimulation. After scale averaging, the LFP-EMG after stimulation was lower than that before stimulation, and the EMG-LFP after stimulation was higher than that before stimulation.Conclusion: There is a significant correlation between NTB and time scale before and after LIPUS,as well as upward and downward. Consequently,This study used FCMC methods to study different NTBs and multi-scale relationships, provides new variables from LIPUS parameters and analysis, and provides new reference for clinical applications of LIPUS.

The fungal octaketide deoxyverrucosidin shares the same α-pyrone core with several nonaketides, including aurovertins, citreoviridin, and asteltoxin. Deoxyverrucosidin features a unique epoxytetrahydrofuran ring. In this study, we demonstrate that this ring system is formed via a flavin-containing monooxygenase-mediated epoxidation on the polyene chain, followed by rearrangement with an epoxide expandase and a second epoxidation on the resulting 2,5-dihydrofuran ring with a cytochrome P450 enzyme. This catalytic cascade differs clearly from the formation of dioxybicyclooctane or tetrahydrofuran motifs in other α-pyrone-containing metabolites, involving one flavin-containing monooxygenase and one hydrolase for up to two rounds of epoxide ring formation and expansion.

This study aims to elucidate Lycium barbarum (LB)'s anti-fatigue mechanisms. Meta-analysis confirmed LB's anti-fatigue capacity, while network pharmacology, molecular docking, and molecular dynamics simulations identified key targets (SRC, HSP90AA1, EGFR, PRKACA, MAPK1). Furthermore, validation experiments in C2C12 cells demonstrated that LB mitigates H2O2-induced reactive oxygen species (ROS) accumulation and restores cell viability. qPCR analysis further revealed that LB downregulates the mRNA expression of CAT, IL-6 and TNF-α, while modulating the expression of these target genes. In summary, our data confirm the anti-fatigue effects of LB and elucidate that LB exerts multi-component, multi-target, and multi-pathway mechanisms in combating fatigue.

Exploring brain function is crucial for unraveling the pathological mechanism underlying stroke. While most studies focus on brain function and emphasize dynamic connections and interactions within or between brain regions, they often ignore the global properties of large-scale network topology. In this study, we analyzed resting-state electroencephalography (EEG) microstates in stroke patients, calculating key parameters such as mean duration (MD), occurrence (OC), time coverage (TC), and transition probability (TP) across different microstate classes. As a result, we identified four microstate classes (A-D) in both healthy subjects and stroke patients. Notably, stroke patients showed significant changes in Classes B-D, with increased MD, OC, and TC in Classes B and C and decreased MD, OC, and TC in Class D. In addition, stroke patients displayed higher TP between Classes B and C than healthy controls. Moreover, we observed a positive correlation between the OC of Class D and clinical Fugl-Meyer scores, suggesting a link between microstate dynamic and motor recovery. This study highlights the connection between specific microstates and brain regions, providing evidence that stroke patients demonstrate increased activity in visual and salience networks (SNs), but decreased activity in the dorsal attention network (DAN). We speculate these results from changes in the occipital lobe, frontal lobe, parietal lobe, and dorsal anterior cingulate cortex. These findings deepen our understanding of stroke pathophysiology and support further research.

This study aimed to investigate the effects of caffeic acid (CA) on the inflammatory response induced by hydrogen peroxide (H 2 O 2 ) in porcine small intestinal epithelial cells (IPEC-J2 cells) and to elucidate the potential molecular mechanisms involved. Firstly, we treated IPEC-J2 cells with different concentrations of H 2 O 2 to establish the inflammation model caused by oxidative stress. Subsequently, we treated IPEC-J2 cells with CA and/or H 2 O 2 to investigate the effect of CA on the inflammatory response of IPEC-J2 cells induced by H 2 O 2. In addition, IPEC-J2 cells were treated with a nuclear factor kappa-B (NF-κB) inhibitor and a Nucleotide-binding Oligomerization Domain (NOD)-like receptor thermal protein domain associated protein 3 (NLRP3) inhibitor, so as to investigate the molecular mechanism by which CA alleviates H 2 O 2 -induced damage in porcine intestinal epithelial cells. The changes in cell morphology, intestinal epithelial cell damage and the expression of genes related to the NF-κB/NLRP3 signalling axis were examined. The results showed that CA attenuated H 2 O 2 -induced intestinal epithelial cell injury, and the mechanism may be related to the inhibition of NF-κB-mediated NLRP3 inflammasome activation. These findings were expected to provide a theoretical basis for more reasonable and effective application of CA, and provide new ideas for nutritional regulation measures to alleviate intestinal inflammation in piglets.

This study examined the impact of dietary pterostilbene (PTS) on pork color and its underlying mechanisms in finishing pigs. Pigs were fed a basal diet or diets supplemented with 25, 50, 100, or 200 mg/kg PTS. It was found that PTS dietary supplementation at 50-200 mg/kg enhanced the redness of the longissimus thoracis (LT) muscle at 45 min post-slaughter and during one week of storage. Additionally, PTS upregulated myoglobin (Mb) protein expression, increased OxyMb proportions, and decreased MetMb proportions. Molecular docking and dynamics simulations demonstrated a strong binding affinity of PTS to Mb, potentially stabilizing the structure of Mb. Furthermore, PTS likely activated the Keap1/Nrf2 pathway by interacting with the Cys151 residue of Keap1, thereby enhancing muscle antioxidant capacity in LT muscle. In conclusion, our results indicate that dietary PTS supplementation improves pork redness by promoting Mb expression, stabilizing Mb structure, and regulating its redox status in finishing pigs.

Myocardial infarction (MI) is a leading cause of morbidity and mortality globally, primarily due to oxidative stress-induced cardiomyocyte apoptosis and adverse cardiac remodeling. OL-FS13, a neuroprotective peptide derived from Odorrana livida, has previously shown anti-apoptotic effects in cerebral ischemia models. However, its role in myocardial protection remains unclear. In this study, we investigated the cardioprotective effects of OL-FS13 in both in vitro and in vivo models of MI. Hydrogen peroxide (H₂O₂) was used to induce oxidative stress in primary neonatal rat cardiomyocytes, while permanent ligation of the left anterior descending (LAD) coronary artery was employed to establish a murine MI model. OL-FS13 treatment significantly attenuated cardiomyocyte apoptosis, reduced ROS accumulation, improved left ventricular function, and decreased infarct size. Mechanistically, OL-FS13 activated the Nrf2/HO-1 signaling pathway, restoring antioxidant protein levels and suppressing oxidative stress-induced apoptosis. Pharmacological inhibition of Nrf2 with ML385 abrogated the antioxidant and anti-apoptotic effects of OL-FS13 both in vitro and in vivo, confirming the central role of this pathway. These findings demonstrate that OL-FS13 exerts potent cardioprotective effects via Nrf2/HO-1 pathway activation and ROS suppression, suggesting its potential as a novel therapeutic agent for the treatment of myocardial infarction.

This study investigated the effects of L-theanine on muscle drip loss, glycolysis, and cytoskeletal protein expression while elucidating its underlying mechanisms. Results demonstrated that diquat-induced oxidative stress exacerbated muscle drip loss by impairing cellular water balance. Diquat significantly increased reactive oxygen species (ROS), malondialdehyde (MDA) and corticosterone (CORT) content in serum, while suppressing serum antioxidant enzyme activities and nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream target genes expression in gastrocnemius (GAS) muscle of mice. Furthermore, diquat disrupted muscle structural integrity, upregulated glycolytic enzyme activities and glycolysis-related gene expression, while inhibiting cal-pain activity, desmin degradation and the expression of calpain 1 (CAPN1), CAPN2, and integrin (31. In addition, diquat significantly upregulated hypoxia-inducible factor 1 alpha (HIF-1 alpha) and glucocorticoid receptor alpha (GR alpha) expression. Dietary L-theanine supplementation effectively decreased muscle drip loss, increased antioxidant capacity and the expression of Nrf2-related signaling molecules, while decreasing muscle glycolysis. It also decreased the expression of desmin, HIF-1 alpha and GR alpha, and increased calpain activity and the expression of CAPN1, CAPN2, and integrin (31 in GAS muscle of diquat-stressed mice. In conclusion, L-theanine alleviated diquat-induced oxidative stress, glycolytic dysregulation and abnormal cytoskeletal protein degradation, thereby reducing drip loss, and the effect might be related to the inhibition of HIF-1 alpha and GR alpha expression.

Heat stress (HS) induces intestinal injury in animals, but the underlying mechanisms are unknown. This study aimed to investigate the protective effect of taurine (TAU) on intestinal injury induced by heat stress. The heat stress model was established by maintaining mice in a constant temperature and humidity environment (41 ± 1 °C, relative humidity 50 %-60 %), with core body temperature reaching 42 °C. In the experimental design, we supplemented different doses (100, 200, and 400 mg/kg) of TAU to the mice's basal diet, while setting up two positive control groups that received intraperitoneal injections of N-acetyl-L-cysteine (NAC) and 4-phenylbutyric acid (4-PBA), respectively. The findings revealed that heat stress led to a significant upregulation of intestinal heat shock protein 70 protein expression along with higher serum corticosterone in mice. Heat stress impaired intestinal morphology, downregulated tight junction protein gene expression and increased intestinal permeability. Simultaneously, heat stress significantly decreased intestinal antioxidant capacity, caused mitochondrial dysfunction, increased the content of inflammatory cytokines and promoted apoptosis, resulting in excessive accumulation of reactive oxygen species (ROS) and triggering endoplasmic reticulum stress. However, dietary supplementation with TAU alleviated these heat stress-induced effects, and similar results were also obtained with NAC and 4-PBA. Together, TAU could inhibit the accumulation of ROS and endoplasmic reticulum stress by enhancing intestinal antioxidant capacity, decreased inflammatory responses and apoptosis, which may exert its protective effect against heat stress-induced intestinal injury.