The mitochondrion is also a major site for maintaining redox homeostasis between reactive oxygen species (ROS) generation and scavenging. The quantity, quality, and functional integrity of mitochondria are crucial for regulating intracellular homeostasis and maintaining the normal physiological function of cells. The role of oxidative stress in human disease is well established, particularly in inflammatory bowel disease and gastrointestinal mucosal diseases. Oxidative stress could result from an imbalance between ROS and the antioxidative system. Mitochondria are both the main sites of production and the main target of ROS. It is a vicious cycle in which initial ROS-induced mitochondrial damage enhanced ROS production that, in turn, leads to further mitochondrial damage and eventually massive intestinal cell death. Oxidative damage can be significantly mitigated by mitophagy, which clears damaged mitochondria. In this review, we aimed to review the molecular mechanisms involved in the regulation of mitophagy and oxidative stress and their relationship in some intestinal diseases. We believe the reviews can provide new ideas and a scientific basis for researching antioxidants and preventing diseases related to oxidative damage.

During weaning, piglets are susceptible to intestinal injuries caused by a range of infections, which has serious economic losses for pig production. Caffeic acid (CA) is a plant-derived phenolic acid that exhibits potential as a dietary supplement for enhancing intestinal health. There is, however, limited information available about the potential benefits of CA supplementation on intestinal injury and growth performance in piglets. A 28-day study was conducted to examine the effectiveness of CA supplementation in protecting against intestinal injury induced by lipopolysaccharide (LPS) in piglets. Twenty-four piglets were randomly divided into 4 groups: control group, LPS group, LPS + CA group, and CA group. Piglets were administrated with LPS or saline on d21 and d28 of the experiment. Supplementation of CA improved intestinal barrier function in LPS-challenged piglets by enhancing intestinal morphology and integrity, as well as increasing the expression of Claudin-1 and ZO-1. Meanwhile, CA supplementation improved the systemic and colonic inflammation response, oxidative stress, and apoptosis induced by LPS. CA supplementation improved the alpha diversity and structure of intestinal microbiota by increasing the abundance of beneficial microbiota. Additionally, it was found to improve metabolic disorders of colonic bile acids (BAs) and short-chain fatty acids (SCFAs) in LPS-challenged piglets, including an increase in primary BAs and isovalerate. In conclusion, CA supplementation could enhance intestinal integrity and barrier function by modifying intestinal microbiota and its metabolites, which led to a reduction in inflammatory responses, and oxidative stress, and ultimately enhanced growth performance in piglets.

Heat stress influences lipid metabolism independently of nutrient intake. It is not well understood how cholesterol and bile acid (BA) metabolism are affected by heat stress. To investigate the alterations of cholesterol and bile acids when pigs are exposed to short term heat stress, 24 Large White pigs (63.2 ± 9.5 kg body weight, BW) were distributed into one of three environmental treatments: control conditions (CON, 23 °C with ad libitum intake; n = 8), heat stress conditions (HS, 33 °C with ad libitum intake; n = 8), or pair-fed conditions (PF, 23 °C with the same amount to the feed consumed by the HS; n = 8) for three days. Compared with CON pigs, HS pigs reduced the average daily feed intake and average daily gain by 55% and 124%, respectively, and significantly increased rectal temperatures by 0.9 °C and respiration rates more than three-fold. The serum total cholesterol (TC), low-density lipoprotein-cholesterol, and triglycerides (TG) increased (p < 0.05), while hepatic TC, TG, and mRNA of 3-hydroxy-3-methylglutaryl-CoA reductase were reduced on day 3. Furthermore, liver taurine-conjugated BAs (TCBAs), including taurolithocholic acid, taurochenodeoxycholic acid (TCDCA), tauroursodeoxycholic acid, taurohyodeoxycholic acid, and taurocholic acid were elevated in HS pigs compared to CON and PF pigs (p < 0.05), and the level of chenodeoxycholic acid was more significant in the PF group than in the CON and HS groups. The concentration of ursodeoxycholic acid in the serum was higher in HS pigs than CON and PF pigs (p < 0.05), and TCDCA was increased in HS pigs compared with PF pigs (p < 0.05). Altogether, short-term HS reduced hepatic cholesterol levels by decreasing cholesterol synthesis, promoting cholesterol to TCBAs conversion, and cholesterol release to serum in growing pigs. This independently reduced feed intake might serve as a mechanism to protect cells from damage during the early period.

Infants and young animals often suffer from intestinal damage caused by oxidative stress, which may adversely affect their overall health. Hydroxytyrosol, a plant polyphenol, has shown potential in decreasing intestinal oxidative stress, but its application and mechanism of action in infants and young animals are still inadequately documented. This study selected piglets as a model to investigate the alleviating effects of hydroxytyrosol on intestinal oxidative stress induced by diquat and its potential mechanism. Hydroxytyrosol improved intestinal morphology, characterized by higher villus height and villus height/crypt depth. Meanwhile, hydroxytyrosol led to higher expression of Occludin, MUC2, Nrf2, and its downstream genes, and lower expression of cytokines IL-1β, IL-6, and TNF-α. Both oxidative stress and hydroxytyrosol resulted in a higher abundance of Clostridium_sensu_stricto_1, and a lower abundance of Lactobacillus and Streptococcus, without a significant effect on short-chain fatty acids levels. Oxidative stress also led to disorders in bile acid (BA) metabolism, such as the lower levels of primary BAs, hyocholic acid, hyodeoxycholic acid, and tauroursodeoxycholic acid, which were partially restored by hydroxytyrosol. Correlation analysis revealed a positive correlation between these BA levels and the expression of Nrf2 and its downstream genes. Collectively, hydroxytyrosol may reduce oxidative stress-induced intestinal damage by regulating BA metabolism.

Velvet deer are not only a representative special economic animal but also an important part of livestock. With the increasing awareness of international competition for germplasm resources in China, more and more attention has been paid to the protection and utilization of germplasm resources. However, there is poor understanding about velvet deer resources. Therefore, we are providing a comprehensive introduction of Chinese velvet deer germplasm resources from the aspects of ecological distribution, domestication and breeding.