RESUMEN
The search for new probiotics has been regarded as an important approach to improving intestinal health in animals. Bacillus has many advantages, such as strong resistance to harmful external factors, wide distribution, and easy colonization of the intestine. Hence, this study aims to screen for a probiotic Bacillus strain that improves animal intestinal health and to elucidate its probiotic mechanism so as to provide probiotic resources for the development of feed-using probiotic formulations. In this research, a strain of Bacillus was isolated from adult pig feces and named B. tequilensis YB-2. In vitro probiotic experiments showed that B. tequilensis YB-2 had strong acid and bile salt resistance, indicating that this strain can customize in the intestine. To further explore the effect of B. tequilensis YB-2 upon animal intestinal health, DSS-induced murine colitis models were established, and the body weight, colonic morphology, inflammatory cytokines level, and intestinal-barrier- and TLR4/NF-κB-pathway-related protein were determined. The results showed that mice receiving drinking water with 3% DSS were found to develop colitis symptoms, including body weight loss and increased disease activity index (DAI); colon length and microvilli shedding were shortened; tight junctions were disrupted; goblet cells decreased; anti-inflammatory cytokines were inhibited; and pro-inflammatory cytokines and the TLR4/NF-κB signaling pathway were activated. Notably, orally received B. tequilensis YB-2 alleviated symptoms of DSS-induced colitis in mice. The above results indicated that B. tequilensis YB-2 was capable of improving colitis in mice by weakening inflammation and intestinal barrier damage, and its mechanism may involve the TLR4/NF-κB pathway. Overall, this research suggests that B. tequilensis YB-2 has the potential to serve as an animal feed additive to prevent intestinal inflammation.
RESUMEN
Probiotics are a group of active microorganisms that form colonies within the body and alter the composition of the flora in a specific area to provide benefits to the host. In this study, a total of 96 Duroc × Landrace × Yorkshire weaned piglets with an initial body weight (BW) of 8.56 ± 0.53 kg were employed in a randomized complete block design for a 28-day experiment. Pigs were randomly divided into two treatment groups: the control group (CON) and the complex probiotic group (CON + 0.2% probiotics), respectively. The study found that through the 28-day experiment, the average daily gain (ADG) of the complex probiotic group was significantly higher than that of the CON (p < 0.05). However, compared with the CON, the feed conversion efficiency significantly decreased on days 0-14 (p < 0.05). The addition of dietary complex probiotic significantly increased the villus height (VH) of duodenum and ileum, acetate, propionate, butyrate, and total short-chain fatty acids (SCFAs) in feces, and decreased fecal methyl mercaptans, acetic acid, and CO2 (p < 0.05). It concluded that feeding weaned piglets 0.2% complex probiotic increased the VH of duodenum and ileum, as well as changed the content of SCFAs in feces. This ultimately led to an increase in ADG.
RESUMEN
Zinc is the second abundant trace element in the human central nervous system (CNS). Zinc homeostasis is impaired in the elderly population and Alzheimer's disease (AD) patients. Due to the failures of ß-amyloid (Aß)- and microtubule-associated protein tau (MAP-tau, tau)-targeting drugs, many researchers consider AD as a multifactorial disease. Emerging evidence demonstrates that zinc is also widely associated with the development of AD. Zinc dyshomeostasis hypothesis of AD has been proposed. In this review, we summarize the role of zinc in Aß production, protein quality control, redox homeostasis, tau phosphorylation, and BDNF signaling. Due to the multifunctional roles of zinc, when zinc dyshomeostasis occurs, it may influence these different biological activities. Zinc dyshomeostasis could be a therapeutic target for AD treatment. However, there is no consensus on the zinc concentration alteration and the effect of zinc overload or zinc deficiency in AD patients, mouse models and cell lines. Given these significant differences across reported studies, it still needs a long time for clinical application in the treatment of AD.
