Inhibition of TNBS-induced intestinal inflammation in crucian carp (Carassius carassius) by oral administration of bioactive Bioactive food derived peptides.

Intestinal enteritis is a main issue in crucian carp production which results in massive economic loss. Traditional antibiotics used for disease prevention of crucian carp (Carassius carassius) have been banned, thus an alternative approach needs to be identified. In this study, the bioactive peptide was evaluated as a diet supplement for preventing intestinal inflammation in crucian carp. Intestinal inflammation was induced by intrarectal administration of a 2,4,6-trinitrobenzene sulfonic acid (TNBS) solution. The fish samples were fed with different diets for 14 days. The disease activity index (DAI), which included, fish swimming, food intake, anal inflammation, body surface, and ascites was determined daily. Intestine segments were stained with haematoxylin and eosin (H.E.) for histopathological analysis. The expression of cytokines, including interleukin-1ß (IL-1ß), interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), and myeloperoxidase (MPO) in crucian carp were determined. In TNBS-induced groups, the DAI scores were dramatically increased compared to the control group. The histopathological analysis showed that the damage of the fish intestine after the injection of TNBS. The relative expression levels of pro-inflammation cytokines (TNF-α, IL-1ß, IL-8, MPO) were significantly increased compared to the control group on day 1. In the TNBS-induced group feed with a diet supplemented with bioactive peptide, the symptoms of intestinal inflammation were relieved on day 3 and the mRNA expression levels of pro-inflammation cytokines (TNF-α, IL-1ß, IL-8, MPO) were reduced compared to day 1. On day 7, the fish samples enrofloxacin group and bioactive peptide group were recovered from TNBS-induced intestinal inflammation. This study showed that the fish diet supplemented with bioactive peptide could help to prevent and recover from intestinal inflammation. Thus, the bioactive peptide can be used as a replacement for antibiotics to prevent disease in aquaculture production.

Tubeimoside I induces autophagy in HepG2 cells by activating the AMP-activated protein kinase signaling pathway.

Tubeimoside I (TBMS) is a natural compound with antitumor properties. However, the detailed mechanism underlying the function of TBMS in liver cancer has not been fully elucidated. In the present study, TBMS was shown to suppress cell proliferation and induce S phase cell cycle arrest in HepG2 cells. Furthermore, TBMS treatment induced autophagy, evidenced by autophagosome accumulation, and increased the mRNA expression of Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3)-I. However, flow cytometry analysis demonstrated that TBMS exerted no effect on cell apoptosis. Moreover, TBMS increased the phosphorylation of AMP-activated protein kinase (AMPK) in a concentration-dependent manner, thereby activating the AMPK signaling pathway. A specific AMPK inhibitor, compound C (CC), caused markedly suppressed TBMS-induced accumulation of LC3-II. In addition, the mRNA expression of LC3-I and Beclin 1 was also suppressed in cells treated with TBMS and CC in combination. The results of the present study provide new insights into the role of TBMS in inducing autophagy and support the potential application of TBMS for liver cancer treatment in the clinical setting.

Marine microalgae bioengineered Schizochytrium sp. meal hydrolysates inhibits acute inflammation.

Bioengineered marine microalgae Schizochytrium sp. is currently used to produce docosahexaenoic acid (DHA). However, following DHA extraction, the remaining protein-rich materials are not well utilized. In this study, we report that marine microalgae bioengineered Schizochytrium sp. hydrolysate (MESH), which exhibits a unique peptide profile as identified by Ultra Performance Liquid Chromatography coupled with Q-TOF mass spectrometry(UPLC/Q-TOF-MS), ameliorated bowel inflammation in mice. In a mouse model of experimentalcolitis induced by dextran sulfate sodium, compared with the control mice, the mice treated with MESH were highly resistant to colitis, as demonstrated by marked reductions in body weight loss, clinical colitis scores, colonic histological damage, and colonic inflammation. Mechanistically, MESH attenuated the induction of pro-inflammatory cytokines and increased the induction of anti-inflammatory cytokines. MESH also promoted the proliferation of colonic crypt stem cells and progenitor cells required for crypt repair. Collectively, these results reveal a previously unrecognized role of MESH as a potential anti-inflammatory treatment for colitis.