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The liver plays crucial roles in material metabolism and immune response. Bacterial endotoxin can cause various liver diseases, thereby causing significant economic losses to pig industry. Tryptophan is an essential amino acid in piglets. However, whether tryptophan can alleviate liver injury and inflammation by regulating necroptosis and pyroptosis has not been clarified. This study aimed to investigate whether dietary tryptophan can alleviate lipopolysaccharide (LPS)-induced liver injury in weaned piglets. 18 weaned piglets were randomly distributed to three treatments, each with 6 replicates: (1) control; (2) LPS-challenged control; (3) LPS + 0.2% tryptophan. After feeding with control or 0.2% tryptophan-supplemented diets for 35 d, pigs were intraperitoneally injected with saline or LPS (100 mg/kg body weight). At 4 h post-injection, blood samples and liver were collected. Results indicated that tryptophan reduced alanine aminotransferase, aspartate aminotransferase, decreased the mRNA expression and protein expression of 70-kDa heat shock proteins. Moreover, tryptophan increased the mRNA expression and protein expression of claudin-1, occludin and zonula occludens and decreased hydrogen peroxide and malondialdehyde contents, and increased catalase, glutathione peroxidase and total superoxide dismutase activities and proinflammatory cytokine levels in the liver. Meanwhile, tryptophan inhibited pyroptosis-related and necroptosis-related protein expression in liver. Collectively, tryptophan could relieve liver damage, increased the antioxidant capacity and reduced inflammation by inhibiting pyroptosis and necroptosis signaling pathways. [ABSTRACT FROM AUTHOR]

Tryptophan is a functional amino acid. This study aimed to investigate whether dietary tryptophan supplementation can alleviate Escherichia coli lipopolysaccharide (LPS)-induced skeletal muscle fiber transition from type I to type II in pigs, and the molecular mechanism was also examined. Eighteen weaned piglets were allotted to three treatments groups, namely, the nonchallenged control, LPS-challenged control and LPS + 0.2% tryptophan groups. On day 35, the pigs in the LPS and LPS + 0.2% tryptophan groups were challenged by injection with 100 μg/kg body weight (BW) LPS, whereas the control group was given sterile saline. Tryptophan can attenuate LPS-induced decrease in protein content of slow MyHC, the activities of succinic dehydrogenase, malate dehydrogenase (MDH) and antioxidant enzyme, the mRNA expression of oxidative muscle fiber-related genes, type I fiber proportion, and increase in lactate dehydrogenase (LDH) activity, the mRNA expression level of MyHC IIb and type II fiber proportion. Moreover, tryptophan supplementation attenuated LPS-induced decrease in the expression levels of phosphorylated AMP-activated protein kinase (AMPK), silent information regulator 1 (Sirt1) and peroxisome proliferator activated receptor gamma coactivator 1-alpha (PGC-1α). Collectively, tryptophan can alleviate LPS-induced muscle fiber type transformation from type I to type II. This effect is associated with activating the Sirt1/AMPK/PGC-1α signaling pathway. [ABSTRACT FROM AUTHOR]

This study aimed to test the hypothesis that the calcium-sensing receptor (CaSR) can protect intestinal epithelial barrier integrity and decrease inflammatory response mediated by the Ras-related C3 botulinum toxin substrate 1 (Rac1)/phospholipase Cγ1 (PLC-γ1) signaling pathway. IPEC-J2 monolayers were treated without or with TNF-α in the absence or presence of CaSR antagonist (NPS 2143), CaSR overexpression, and Rac1 silencing, PLCγ1 silencing or spermine. Results showed that spermine increased transepithelial electrical resistance (TER), tight junction protein levels, the protein concentration of Rac1/PLC-γ1 signaling pathway, and decreased paracellular permeability in the presence of TNF-α. NPS2143 inhibited spermine-induced change in above-mentioned parameters. CaSR overexpression increased TER, the levels of tight junction proteins and the protein concentration of CaSR, phosphorylated PLCγ1, Rac1, and IP3, and decreased paracellular permeability and contents of interleukin-8 (IL-8) and TNF-α after TNF-α challenge. Rac1 and PLCγ1 silencing inhibited CaSR-induced increase in barrier function and the protein concentration of phosphorylated PLCγ1, Rac1, and IP3, and decrease in contents of IL-8 and TNF-α after TNF-α challenge. These results suggest that CaSR activation protects intestinal integrity and alleviates the inflammatory response by activating Rac1 and PLCγ1 signaling after TNF-α challenge, and spermine can maintain barrier function via CaSR/Rac1/PLC-γ1 pathway. [ABSTRACT FROM AUTHOR]

The rapid healing of impaired intestinal surface plays a role in maintaining intestinal homeostasis. This study investigated the effect of calcium-sensing receptor (CaSR) on the migration and proliferation of intestinal porcine epithelial cells (IPEC-J2). Results showed that cell migration area and width were increased by R568 (CaSR activator) and decreased by NPS2143 (CaSR inhibitor). The protein level of GTP-rac1 and the phosphorylation of phospholipase C gamma 1 (PLCγ1) were increased by 2 µM R568. Furthermore, R568 + 120 µM NSC23766 (Rac1 inhibitor) and R568 + 1 µM U73122 (PLCγ1 inhibitor) decreased the protein level of GTP-rac1 and the phosphorylated PLCγ1, respectively, and both inhibited cell migration compared with R568. In addition, spermine increased the protein expression levels of CaSR and the levels of GTP-rac1 and the phosphorylated PLCγ1 and thereby promoted the migration of IPEC-J2 cells. Moreover, R568 improved the proliferation of the IPEC-J2 cells. Spermine increased cell proliferation, but NPS2143 incubated with spermine decreased cell proliferation compared with the spermine group. This study suggests that CaSR activation increased cell migration by activating Rac1 and PLCγ1 signaling and improved cell proliferation, and both effects were regulated by spermine by activating CaSR. [ABSTRACT FROM AUTHOR]

Whether spermine promotes the repair of porcine intestinal epithelium damage through Ras-related C3 botulinum toxin substrate 1 (Rac1)/phospholipase C-γ1 (PLC-γ1) signaling remains unclear. The current study investigated the effects of spermine addition on the proliferation and migration of IPEC-J2 cells and the effects of Rac1/PLC-γ1 signaling on cell migration. We showed that the inhibitors of Rac1 (NSC-23766) and PLC-γ1 (U73122) reduced cell migration and decreased the protein levels of Rac1 and PLC-γ1 in the cells. Moreover, spermine promoted the proliferation and migration of the IPEC-J2 cells, that is, 1 µM spermine exhibited the best effect, and spermine treatment increased the protein levels of Rac1 and PLC-γ1. Further experiments showed that spermine treatment increased cell migration and enhanced Rac1 and PLC-γ1 protein levels, compared with NSC-23766 and U73122 treatments with spermine. In conclusion, spermine treatment promoted the repair of damaged porcine intestinal epithelium by accelerating cell proliferation and migration mediated by Rac1/PLC-γ1 signaling. [ABSTRACT FROM AUTHOR]

Intestinal epithelial restitution is partly dependent on cell migration, which reseals superficial wounding after injury. Here, we tested the hypothesis that stromal interaction molecule 1(STIM1) regulates porcine intestinal epithelial cell migration by activating transient receptor potential canonical 1 (TRPC1) signaling. Results showed that the knockdown of STIM1 repressed cell migration after wounding, reduced the protein concentration of STIM1 and TRPC1, and decreased the inositol trisphosphate (IP3) content in IPEC-J2 cells (p < 0.05). However, overexpression of STIM1 obtained opposite results (p < 0.05). The inhibition of TRPC1 activity by treatment with SKF96365 in cells overexpressing wild-type and mutant STIM1 attenuated the STIM1 overexpression-induced increase of cell migration, STIM1, TRPC1 and IP3 (p < 0.05). In addition, polyamine depletion caused by α-difluoromethylornithine (DFMO) resulted in the decrease of above-mentioned parameters, and exogenous polyamine could attenuate the negative effects of DFMO on IPEC-J2 cells (p < 0.05). Moreover, the overexpression of STIM1 could rescue cell migration, the protein level of STIM1 and TRPC1, and IP3 content in polyamine-deficient IPEC-J2 cells (p < 0.05). These results indicated that STIM1 could enhance porcine intestinal epithelial cell migration via the TRPC1 signaling pathway. Inhibition of cell migration by polyamine depletion resulted from the reduction of STIM1 activity. [ABSTRACT FROM AUTHOR]

The present work aimed to explore the influence and underlying mechanisms involving arginine in testicular development in boars. To this end, thirty 30‐day‐old male Duroc piglets (7.00 ± 0.30 kg) were randomly sorted into two groups, maintained on either a basal diet (CON, n = 15) or a diet supplemented with 0.8% arginine (ARG, n = 15). Blood and testicular samples were collected during the experimental period to analyse amino acid composition and arginine metabolite levels. The results showed that dietary supplementation with arginine increased number of spermatogonia and height of the seminiferous epithelium (p < 0.05). Sperm density, total number and effective number of sperm of the boars in the ARG group increased significantly compared with those in the CON group (p < 0.05). Although arginine supplementation did not affect plasma amino acid levels, testicular arginine levels in 150‐day‐old boars exhibited a significant increase (p < 0.05). The level of serum nitric oxide (NO) and activity of nitric oxide synthase (NOS) also increased in 150‐day‐old boars in the ARG group (p < 0.05). Interestingly, dietary supplementation with arginine increased testicular levels of putrescine in 150‐day‐old boars (p < 0.05). These results indicated that arginine supplementation increased serum NO levels and testicular arginine and putrescine abundance, thereby improving testicular development and semen quality in boars. [ABSTRACT FROM AUTHOR]