Ileal Protein Content Research Articles

Polyphenols Sourced from Ilex latifolia Thunb. Relieve Intestinal Injury via Modulating Ferroptosis in Weanling Piglets under Oxidative Stress.

Polyphenols sourced from Ilex latifolia Thunb. (PIT) contain high levels of phenolic acids, tannic acids, triterpenoids and so on, which play important roles in antioxidant function. This study was conducted to investigate the effects of PIT against intestinal injury in piglets under oxidative stress. Thirty-two weanling piglets were arranged by a 2 × 2 factorial experiment with diets (basal diet vs. PIT diet) and oxidative stress (saline vs. diquat). All piglets were injected with saline or diquat on d 21, respectively. After 7 days, all pigs were slaughtered and intestinal samples were collected. PIT enhanced jejunal villus heights and crypt depth in the piglets under oxidative stress. PIT increased the activities of intestinal mucosal lactase, sucrase and maltase in the challenged piglets. PIT also increased the jejunal ratio of protein to DNA and ileal protein content. PIT increased the jejunal activities of GSH-PX and GSH content and reduced the ileal MDA amounts. Furthermore, PIT regulated the expression of ferroptosis mediators, such as TFR1, HSPB1, SLC7A11 and GPX4. These results indicate that dietary PIT supplementation enhances the histological structure and function of the intestinal mucosa, which is involved in modulating antioxidant capacity and ferroptosis.

Glycine Relieves Intestinal Injury by Maintaining mTOR Signaling and Suppressing AMPK, TLR4, and NOD Signaling in Weaned Piglets after Lipopolysaccharide Challenge

This study was conducted to envaluate whether glycine could alleviate Escherichia coli lipopolysaccharide (LPS)-induced intestinal injury by regulating intestinal epithelial energy status, protein synthesis, and inflammatory response via AMPK, mTOR, TLR4, and NOD signaling pathways. A total of 24 weanling piglets were randomly allotted to 1 of 4 treatments: (1) non-challenged control; (2) LPS-challenged control; (3) LPS + 1% glycine; (4) LPS + 2% glycine. After 28 days feeding, piglets were injected intraperitoneally with saline or LPS. The pigs were slaughtered and intestinal samples were collected at 4 h postinjection. The mRNA expression of key genes in these signaling pathways was measured by real-time PCR. The protein abundance was measured by Western blot analysis. Supplementation with glycine increased jejunal villus height/crypt depth ratio. Glycine also increased the jejunal and ileal protein content, RNA/DNA ratio, and jejunal protein/DNA ratio. The activities of citroyl synthetase in ileum, and α-ketoglutarate dehydrogenase complex in jejunum, were increased in the piglets fed diets supplemented with glycine. In addition, glycine decreased the jejunal and ileal phosphorylation of AMPKα, and increased ileal phosphorylation of mTOR. Furthermore, glycine downregulated the mRNA expression of key genes in inflammatory signaling. Meanwhile, glycine increased the mRNA expression of negative regulators of inflammatory signaling. These results indicate that glycine supplementation could improve energy status and protein synthesis by regulating AMPK and mTOR signaling pathways, and relieve inflammation by inhibiting of TLR4 and NOD signaling pathways to alleviate intestinal injury in LPS-challenged piglets.

P21 (WAF1/CIP1) is required for the mitogenic response to intestinal resection.

Increased enterocyte proliferation and apoptosis characterize the intestinal adaptive response to massive small bowel resection (SBR). Since p21 (WAF1/CIP1) has been implicated to play a role in cellular differentiation and apoptosis, this study tested the hypothesis that p21 is obligatory for adaptation to occur. p21-null (n = 36) and wild-type (C57B1/6, n = 19) mice underwent a 50% SBR or sham operation. After 3 days, parameters of adaptation (ileal wet weight, villus/crypt morphology, and ileal protein content), an enterocyte proliferation index (PI), and an apoptotic index (AI) were determined in the residual ileum. In a separate set of experiments, p21-null (n = 11) and control (n = 20) mice underwent the aforementioned operative procedures and the remnant intestine was subjected to a reverse transcription polymerase chain reaction for p27 (KIP1). Both AI and PI increased after SBR in the wild-type mice. In the p21-null mice, SBR increased AI, but did not affect the PI. After SBR, adaptive parameters increased in the wild-type mice, but failed to increase in the p21-null mice. The absence of p21 caused a baseline increase in p27 mRNA, which did not change after SBR. p21 appears to be required to increase enterocyte proliferation and to augment the other parameters of intestinal adaptation. In the absence of p21, the proliferative and apoptotic responses to SBR are uncoupled. These results suggest a differential mechanism for the regulation of enterocyte proliferation and apoptosis in the adapting intestine.