Yucca schidigera purpurea-sourced arabinogalactan polysaccharides augments antioxidant capacity facilitating intestinal antioxidant functions.

This study isolated and purified a novel homogeneous arabinogalactan polysaccharide from Yucca schidigera extract (YSE), unveiled its unique structure and explored its antioxidant function. Firstly, the antioxidant potential of YSE was demonstrated in piglet trials. A homogeneous polysaccharide with a molecular weight of 24.2 kDa, designated as Yucca schidigera polysaccharide B (YPB), was isolated and purified from YSE. The monosaccharide composition of YPB was Rha, Araf, Galp, and Glcp, whose molar percentages were 2.8 %, 11.6 %, 45.5 %, and 40.0 %, respectively. Methylation analysis combined with 1D and 2D nuclear magnetic resonance showed that YPB was a complex polysaccharide with a main glycosidic linkage pattern of →2)-α-ʟ-Rha-(1 â†’ 3)-ß-ᴅ-Galp-(1→3)-ß-ᴅ-Galp-(1 â†’ 3)-ß-ᴅ-Galp-(1 â†’ 3)-ß-ᴅ-Glcp-(1→, and branched Araf and Galp fragments were connected with the main chain through →3,6)-ß-ᴅ-Galp-(1→, →3,4)-ß-ᴅ-Glcp-(1→, and →2,4)-α-ʟ-Rha-(1→ linkages. Following the in vitro biochemical assays of bioactive components, YPB should be the contributor to the antioxidant activity in YSE. Based on the establishment of oxidative stress model, YPB exhibited strong antioxidant capacity and activated NRF2 pathway, and then provided protection against the damage induced oxidative stress in IPEC-J2 cells and rats. Further analysis with inhibitors found that this antioxidant effect was attributed to its interaction with epidermal growth factor receptor and mannose receptor, and stimulating PI3K/AKT pathway.

Yucca schidigera extract decreases nitrogen emission via improving nutrient utilisation and gut barrier function in weaned piglets.

Yucca schidigera extract (YE) can decrease ammonia concentration in livestock housing, which could be associated with the inhibition of urease. The aim of this study was to investigate the other possible reasons of dietary YE supplementation reducing nitrogen emission in weaned piglets. A total of 14 crossbred weaned barrows were allotted into two groups fed the diets supplementing 0 and 120 mg/kg YE for 14 days. The YE administration decreased F/G ratio and hindgut NH3 -N production in weaned piglets (p < 0.05). Dietary YE supplementation decreased serum urea nitrogen levels, and increased nutrient digestibility, which could be related to the improvement of morphology, digestive and absorptive enzyme activities, and nutrient transporter mRNA expression in jejunal mucosa of weaned piglets (p < 0.05). The mRNA expression of tight junction proteins, mucins and apoptosis-related genes was also improved by YE treatment in jejunal mucosa of weaned piglets (p < 0.05). In addition, dietary YE supplementation regulated the microbiota structure and volatile fatty acid content in distal intestine of weaned piglets (p < 0.05). These results suggest that YE administration can decrease hindgut NH3 -N production in weaned piglets, which is associated with the increased nutrient utilization and gut-barrier function.

Tea bioactive components prevent carcinogenesis via anti-pathogen, anti-inflammation, and cell survival pathways.

Cancer seriously impairs human health and survival. Many perturbations, such as increased oxidative stress, pathogen infection, and inflammation, promote the accumulation of DNA mutations, and ultimately lead to carcinogenesis. Tea is one of the most highly consumed beverages worldwide and has been linked to improvements in human health. Tea contains many active components, including tea polyphenols, tea polysaccharides, L-theanine, tea pigments, and caffeine among other common components. Several studies have identified components in tea that can directly or indirectly reduce carcinogenesis with some being used in a clinical setting. Many previous studies, in vitro and in vivo, have focused on the mechanisms that functional components of tea utilized to protect against cancer. One particular mechanism that has been well described is an improvement in antioxidant capacity seen with tea consumption. However, other mechanisms, including anti-pathogen, anti-inflammation and alterations in cell survival pathways, are also involved. The current review focuses on these anti-cancer mechanisms. This will be beneficial for clinical utilization of tea components in preventing and treating cancer in the future.

Tea and Its Components Prevent Cancer: A Review of the Redox-Related Mechanism.

Cancer is a worldwide epidemic and represents a major threat to human health and survival. Reactive oxygen species (ROS) play a dual role in cancer cells, which includes both promoting and inhibiting carcinogenesis. Tea remains one of the most prevalent beverages consumed due in part to its anti- or pro-oxidative properties. The active compounds in tea, particularly tea polyphenols, can directly or indirectly scavenge ROS to reduce oncogenesis and cancerometastasis. Interestingly, the excessive levels of ROS induced by consuming tea could induce programmed cell death (PCD) or non-PCD of cancer cells. On the basis of illustrating the relationship between ROS and cancer, the current review discusses the composition and efficacy of tea including the redox-relative (including anti-oxidative and pro-oxidative activity) mechanisms and their role along with other components in preventing and treating cancer. This information will highlight the basis for the clinical utilization of tea extracts in the prevention or treatment of cancer in the future.

[Discovery of a new splicing type of KCHIP1 gene].

The present study aimed to find the mutations of KCHIP1 gene in breast cancer. KCHIP1 cDNA samples from 12 specimens of breast cancer and 12 specimens of normal mammary tissues were amplified by reverse transcription-polymerase chain reaction (RT-PCR), and directly sequenced to detect mutation. No mutation of KCHIP1 gene was found in these samples; while a new splicing type of KCHIP1 gene was found, which has an insert (162 bp) between exon 1 and exon 2 in KCHIP1 gene (AY780424).