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Liubao tea (LBT) is a unique microbial‐fermented tea that boasts a long consumption history spanning 1500 years. Through a specific post‐fermentation process, LBT crafted from local tea cultivars in Liubao town Guangxi acquires four distinct traits, namely, vibrant redness, thickness, aging aroma, and purity. The intricate transformations that occur during post‐fermentation involve oxidation, degradation, methylation, glycosylation, and so forth, laying the substance foundation for the distinctive sensory traits. Additionally, LBT contains multitudinous bioactive compounds, such as ellagic acid, catechins, polysaccharides, and theabrownins, which contributes to the diverse modulation abilities on oxidative stress, metabolic syndromes, organic damage, and microbiota flora. However, research on LBT is currently scattered, and there is an urgent need for a systematical recapitulation of the manufacturing process, the dominant microorganisms during fermentation, the dynamic chemical alterations, the sensory traits, and the underlying health benefits. In this review, current research progresses on the peculiar tea varieties, the traditional and modern process technologies, the substance basis of sensory traits, and the latent bioactivities of LBT were comprehensively summarized. Furthermore, the present challenges and deficiencies that hinder the development of LBT, and the possible orientations and future perspectives were thoroughly discussed. By far, the productivity and quality of LBT remain restricted due to the reliance on labor and experience, as well as the incomplete understanding of the intricate interactions and underlying mechanisms involved in processing, organoleptic quality, and bioactivities. Consequently, further research is urgently warranted to address these gaps. [ABSTRACT FROM AUTHOR]

This study aimed to explore the protective effects of L-theanine supplementation on the diquat-challenged weaned piglets. A total of 160 weaned piglets were randomly divided into 4 groups using a 2 × 2 two-factor design, there were 4 replicates per group and 10 pigs per replicate. Piglets were fed diets (with 1000 mg/kg L-theanine addition or not), then challenged with diquat or saline on day 7. 21 days after challenge, two pigs from each replicate were selected for sample collection. Results showed that supplement with 1000 mg/kg L-theanine down-regulated the diarrhea rate, serum D-lactate level, tumor necrosis factor-α, and phosphorylation of extracellular regulated protein kinases (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK) signaling in pigs without diquat challenge (p < 0.05). While for diquat-challenged piglets, L-theanine addition increased average daily gain, jejunum villus height, and interferon-γ level (p < 0.05). Meanwhile, L-theanine addition decreased the diarrhea rates and mortality, serum D-lactate level, and phosphorylation of ERK and JNK in diquat-challenged pigs (p < 0.05). These results demonstrate that L-theanine pretreatment could alleviate diquat-induced oxidative stress and improve intestinal barrier function in diquat-challenged weaned piglets, which can be attributed to suppression of MAPK phosphorylation signaling pathways. [ABSTRACT FROM AUTHOR]

BACKGROUND: Oxidative stress plays an important role in femoral head necrosis. Platelet-rich plasma (PRP) contains growth factors that can accelerate fracture healing. PRP combined with core decompression can promote recovery from non-traumatic femoral head necrosis. OBJECTIVE: To investigate whether PRP combined with core decompression can inhibit oxidative stress in steroid-induced avascular necrosis of the femoral head model via Keap1/Nrf2/HO-1 signaling pathway. METHODS: Forty New Zealand rabbits were randomly divided into normal group, model group, control group and PRP group, with 10 rabbits in each group. In the model and PRP groups, a model of steroid-induced femoral head necrosis was established in a sterile environment. At 4 weeks after operation, the rabbits in the PRP group were injected with 0.4 mL of 3% PRP after core decompression. The control group received core decompression treatment, and the control and model groups were raised normally. After 14 weeks, the experimental animals were sacrificed. Hematoxylin-eosin staining was used to observe the pathological changes of bone marrow cavity and the vacancy rate of bone lacunae in the femoral head of each group. Total antioxidant capacity, superoxide dismutase, glutathione peroxidase, reduced glutathione, and malondialdehyde were detected. TUNEL was used to detect bone cell apoptosis in the femoral head. Immunofluorescence staining was used to determine the distribution of Keap1 and Nrf2. Western blot was used to measure Keap1, Nrf2, and H0-1 protein expression in the femoral head. Approval was obtained from the Animal Ethics Committee of the Affiliated Hospital of Qinghai University, approval No. qhdx-201908374. RESULTS AND CONCLUSION: (1) Compared with the normal group, the trabecular bone in model group was thinned with structure disorder. Compared with the model group, the trabecular bone structure in control group was restored, and the number of vacant bone lacunae was reduced (P < 0.05). Compared with the control group, the animals treated with PRP combined with core decompression were further improved, the trabecular bone structure was further improved, and the number of vacant bone lacunae was further reduced (P < 0.05). Whereas there was no significant difference between the PRP group and normal group (P > 0.05). (2) The total antioxidant capacity and serum levels of superoxide dismutase, glutathione peroxidase, and reduced glutathione in the model group were significantly lower than those in normal animals (P < 0.05), while the MDA concentration was significantly higher than that in the normal group (P < 0.05). These oxidative stress indexes were slightly improved in the control group compared with the model group (P > 0.05), while these indexes were significantly improved in the PRP group than the model and control groups (P < 0.05). (3) The expression of Kesp1 in the model group was significantly lower than that of the normal group (P < 0.05), and the expression of Nrf2 and HQ-1 protein was significantly higher than that of the normal group (P < 0.05). The expression of Keap1 in the PRP group was lower than that of the model and control groups (P < 0.05), and the expression of Nrf2 and HQ-1 was significantly higher than that of the model and control groups (P < 0.05). Therefore, PRP can effectively inhibit oxidative stress in the process of steroid-induced femoral head necrosis, which may be caused by activating the Keap1/Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]