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Extensive research from large prospective cohort studies and meta-analytical investigations over recent decades have consistently indicated that dairy foods have protective effects, reducing the risk of colorectal cancer. Most of the literature has explored the potential role of milk minerals and vitamins in managing colorectal cancer. Yet, there is a paucity of a comprehensive summary of the anticancer attributes of milk protein components and their underlying mechanisms of action. Recent advancements have spotlighted the potential of whey proteins, including β-lactoglobulin, α-lactalbumin, serum albumin, and lactoferrin, as promising candidates for both the prevention and treatment of colorectal cancer. Notably, whey proteins have demonstrated a more pronounced capacity for suppressing carcinogen-induced tumors when compared to casein. Their strong binding affinity enables them to serve as effective carriers for small molecules or drugs targeting colon cancer therapy. Furthermore, numerous studies have underscored the anti-inflammatory and antioxidant prowess of whey proteins in cancer prevention. Additionally, whey proteins have been shown to trigger apoptosis, hinder tumor cell proliferation, and impede metastasis. This comprehensive review, therefore, not only substantiates the significance of incorporating whey protein components into a balanced daily diet but also underscores their potential in safeguarding against the onset and progression of colorectal cancer. HIGHLIGHTS: Dairy products have consistently had protective effects in reducing the risk of colorectal cancer. Whey proteins have shown promise as candidates for the prevention and treatment of colorectal cancer. Whey proteins have a strong binding ability, enabling them to act as carriers of small molecules or drugs targeting colon cancer therapy. Their anti-inflammatory and anti-oxidant capacity may play a role in cancer prevention. Whey proteins could induce apoptosis and inhibit the proliferation and metastasis of tumor cells. [ABSTRACT FROM AUTHOR]

NLRP3 inflammasome plays a critical spatiotemporal role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE). This study reports a mechanistic insight into noncanonical NLRP3 inflammasome activation in microglia for the effector stage of EAE. Microglia-specific deficiency of ASC (apoptosis-associated speck-like protein containing a C-terminal caspase-activation and recruitment [CARD] domain) attenuated T cell expansion and neutrophil recruitment during EAE pathogenesis. Mechanistically, TLR stimulation led to IRAKM-caspase-8-ASC complex formation, resulting in the activation of caspase-8 and IL-1[beta] release in microglia. Noncanonical inflammasome-derived IL- 1[beta] produced by microglia in the CNS helped to expand the microglia population in an autocrine manner and amplified the production of inflammatory cytokines/chemokines. Furthermore, active caspase-8 was markedly increased in the microglia in the brain tissue from patients with multiple sclerosis. Taken together, our study suggests that microglia-derived IL-1[beta] via noncanonical caspase-8-dependent inflammasome is necessary for microglia to exert their pathogenic role during CNS inflammation., IntroductionNumerous studies indicate that the inflammatory process in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is initiated by T cells that are reactive against myelin (1-6). Importantly, a growing [...]

Simple Summary: Digestibility is a crucial factor for assessing feed costs for dairy cattle. Rapid analysis of fecal composition is necessary to obtain accurate data on digestive efficiency. Traditional wet chemical analysis methods are time-consuming; therefore, the potential of near-infrared reflectance spectroscopy technique was explored for assessing fecal chemical components in dairy cattle. The technique has been widely used to predict the nutritional contents of raw materials and complete feeds. In the present study, near-infrared reflectance spectroscopy could successfully predict the chemical composition of dairy cattle feces, thereby reducing analysis time and workload. Traditional methods for determining the chemical composition of cattle feces are uneconomical. In contrast, near-infrared reflectance spectroscopy (NIRS) has emerged as a successful technique for assessing chemical compositions. Therefore, in this study, the feasibility of NIRS in terms of predicting fecal chemical composition was explored. Cattle fecal samples were subjected to chemical analysis using conventional wet chemistry techniques and a NIRS spectrometer. The resulting fecal spectra were used to construct predictive equations to estimate the chemical composition of the feces in both cows and calves. The coefficients of determination for calibration (RSQ) were employed to evaluate the calibration of the predictive equations. Calibration results for cows (dry matter [DM], RSQ = 0.98; crude protein [CP], RSQ = 0.93; ether extract [EE], RSQ = 0.91; neutral detergent fiber [NDF], RSQ = 0.82; acid detergent fiber [ADF], RSQ = 0.89; ash, RSQ = 0.84) and calves (DM, RSQ = 0.92; CP, RSQ = 0.89; EE, RSQ = 0.77; NDF, RSQ = 0.76; ADF, RSQ = 0.92; ash, RSQ = 0.97) demonstrated that NIRS is a cost-effective and efficient alternative for assessing the chemical composition of dairy cattle feces. This provides a new method for rapidly predicting fecal chemical content in cows and calves. [ABSTRACT FROM AUTHOR]

Simple Summary: During pregnancy, especially the perinatal period, cows are often in a state of negative energy balance due to the imbalance of glucose metabolism. As the main energy substrate to promote fetal development, glucose is mainly obtained from the mother through the placenta and the provision of glucose to the fetus depends on the activity of glucose transporters distributed within the placental tissue. As the basic component of placental tissue, placental trophoblast cells participate in nutrient supply and metabolism between mother and fetus. However, a noticeable void exists in the study of the function and potential regulation mechanism of placental trophoblast cells in ruminants. In light of this, the bovine placental trophoblast cells were treated with different dose-concentration glucose and the gene expression of glucose transport carriers and enzymes related to glucose metabolism were detected. Moreover, the signaling pathway of placental-sensing energy level changes were studied to explore the mechanism of placenta mediating energy metabolism transmission between mother and fetus. The results showed that glucose regulates cellular glucose transport and metabolism by mediating the mTOR signaling pathway in bovine placental trophoblast cells. It has been confirmed that improving the energy level of the diet contributed to the greater reproductive performance and birth weight of calves in periparturient dairy cows. To investigate the effect of glucose on nutrient transport during fetal development, the bovine placental trophoblast cells (BPTCs) were cultured in media with different glucose concentrations (1, 2, 4, 8, or 16 mg/mL). Subsequently, the BPTCs were cultured in media with 1, 8 mg/mL glucose and 8 mg/mL glucose plus 100 nmol/L rapamycin (the inhibitor of mTOR pathway). Compared with the 1 mg/mL glucose, the addition of 8 mg/mL glucose stimulated cell proliferation, upregulated the mRNA abundance of the glucose transporter GLUT1 and GLUT4, and increased the activity of glucose metabolism-related enzyme glucose-6-phosphate dehydrogenease (G6PD), lactate dehydrogenase (LDHA) and phosphoglycerate kinase 1 (PGK1), as well as adenosine-triphosphate (ATP) content (p < 0.05).Furthermore, compared with the treatment of 1 mg/mL glucose, adding 8 mg/mL of glucose-upregulated gene expression in the mTOR signaling pathway, including phosphatidylinositol3-kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR) and 70 kDa ribosomal protein S6 kinase 2 (P70S6K) (p < 0.05).The supplementation of rapamycin downregulated the gene and protein expression of the mTOR signaling pathway, including mTOR, P70S6K, EIF4E-binding protein 1 (4EBP1), hypoxia-inducible factor 1-alpha (HIF-1α) and gene expression of glucose transporter upregulated by 8 mg/mL glucose (p < 0.05). Thus, these results indicated that the addition of 8 mg/mL glucose regulated the glucose transport and metabolism in BPTCs through the mTOR signaling pathway, thereby promoting the supply of nutrients to fetus. [ABSTRACT FROM AUTHOR]