Search

Liaoyu white cattle (LYWC) is a local breed in Liaoning Province, China. It has the advantages of grow quickly, high slaughter ratew, high meat quality and strong anti-stress ability. N6 methyladenosine (m6A) is a methylation modification of N6 position of RNA adenine, which is an important modification mechanism affecting physiological phenomena. In this study, we used the longissimus dorsi muscle of LYWC and SIMC for m6A-seq and RNA-seq high-throughput sequencing, and identified the key genes involved in muscle growth and m6A modification development by bioinformatics analysis. There were 31532 m6A peaks in the whole genome of LYWC and 47217 m6A peaks in the whole genome of SIMC. Compared with Simmental cattle group, LYWC group had 17,351 differentially expressed genes: 10,697 genes were up-regulated, 6,654 genes were down regulated, 620 differentially expressed genes were significant, while 16,731 differentially expressed genes were not significant. Among the 620 significantly differentially expressed genes, 295 genes were up-regulated and 325 genes were down regulated. In order to explore the relationship between m6A and mRNA expression in the muscles of LYWC and SIMC, the combined analysis of MeRIP-seq and RNA-seq revealed that 316 genes were m6A modified with mRNA expression. To identify differentially methylated genes related to muscle growth, four related genes were selected for quantitative verification in LYWC and SIMC. GO enrichment and KEGG analysis showed that the differentially expressed genes modified by m6A are mainly involved in skeletal muscle contraction, steroid biosynthesis process, redox process, PPAR pathway and fatty acid metabolism, and galactose metabolism. These results provide a theoretical basis for further research on the role of m6A in muscle growth and development.

This study assessed the protective mechanism of astaxanthin (ASX) against ochratoxin A- (OTA-) induced cardiac injury in mice. Four groups of mice were established: control group (0.1 mL olive oil+0.1 mL NaHCO2), OTA group (0.1 mL OTA 5 mg/kg body weight), ASX group (0.1 mL ASX 100 mg/kg body weight), and ASX + OTA group (0.1 mL ASX 100 mg/kg body weight, 2 h later, 0.1 mL OTA 5 mg/kg body weight). The test period lasted for 27 days (7 days of dosing, 2 days of rest). Electrocardiogram, body weight, heart weight, tissue pathology, oxidative markers (malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH)), biochemical markers (creatine kinase (CK), creatine kinase isoenzyme (CK-MB), and lactate dehydrogenase (LDH)), electron microscopy, TUNEL, and Western blot tests were used to examine the effects of OTA on myocardial injury and ASX detoxification. The results showed that OTA exposure significantly decreased both body weight and heart weight. OTA induced a decrease in heart rate in mice and decreased tissue concentrations of SOD, CAT, and GSH, while increasing serum concentrations of cardiac enzymes (CK, CK-MB, and LDH) and tissue MDA. ASX improved heart rate, cardiac enzymes, and antioxidant levels in mice. The results of tissue pathology and TUNEL assay showed that ASX protects against OTA-induced myocardial injury. In addition, Western blot results showed that the OTA group upregulated Keap1, Bax, Caspase3, and Caspase9, while it downregulated Nrf2, HO-1, and Bcl-2 protein expression. ASX played a protective role by changing the expression of Keap1, Nrf2, HO-1, Bax, Bcl-2, Caspase3, and Caspase9 proteins. These results indicate that the protective mechanism of ASX on the myocardium works through the Keap1-Nrf2 signaling pathway and mitochondria-mediated apoptosis pathway. This study provides a molecular rationale for the mechanism underlying OTA-induced myocardial injury and the protective effect of ASX on the myocardium.

We investigated the protective effect and mechanism of selenium-enriched yeast (SY) on caecal injury induced by ochratoxin A (OTA) in broilers. Eighty broiler chickens of 1-day-old with similar weight were randomly assigned to Control group, OTA group, SY group and OTA + SY group, and were intragastricaly administered with OTA and SY for 21 consecutive days. The results showed that SY could reduce the caecal pathological injuries and could inhibit oxidative stress caused by OTA exposure. The OTA + SY group showed a statistically significant (p 0.01) reduction in the level of MDA, IL-1β, IL-6 and IFN-γ, whereas the levels of GSH, SOD activity and IL-10 were significantly increased (p 0.01). By regulating TLR4/MYD88 signaling pathway, SY inhibited the expression of NF-κB, increased the expression of tight junction-related genes Claudin-1, Occludin and ZO-1, and antagonized the intestinal barrier injury caused by OTA exposure. Moreover, the microbial diversity analyses indicated that SY could intervene changes in the diversity of gut microbiota and the imbalance of gut microbiota caused by OTA. SY could relieve caecal pathological injuries, alleviate OTA-induced caecal oxidative stress and inflammatory response, increase the gut microbial diversity and protect broiler's intestinal barrier from injury.

The aim of this research was to evaluate the potential protective mechanism of astaxanthin (ASTA) against oxidative damage and inflammation caused by ochratoxin (OTA) in mouse lung. We divided mice into a control group (CG), an OTA group (PG), an astaxanthin group (AG), and an OTA+ASTA group (JG). Oxidative indices (malondialdehyde (MDA), total superoxide dismutase (T-SOD), and reduced glutathione (GSH)) and inflammatory markers (interleukin 1&beta, (IL-1&beta, ), interleukin 6 (IL-6), and tumor necrosis factor &alpha, (TNF-&alpha, )) were assayed in the lung, and the lung-weight-to-body-weight ratio was calculated. Apoptosis was detected in pathological sections by the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Oxidative damage and inflammation were detected in the lung of mice after exposure to OTA. Besides, Nrf2- and NF-&kappa, B-pathway-associated proteins were detected by Western blot. In contrast with OTA, ASTA significantly raised the expression of Nrf2, HO-1, and MnSOD, while the expression of other proteins (Keap1, TLR4, and NF-&kappa, B) was significantly decreased. These results indicate that ASTA exerted protective effects against OTA-induced oxidative damage and inflammation in the lung by regulating the Nrf2 and NF-&kappa, B pathways.