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The oil derived from Psidium guajava seeds (TKSO) exhibits an abundance of diverse unsaturated fatty acids, notably oleic, linoleic, and α-linolenic acids, conferring substantial health advantages in addressing metabolic irregularities and human diseases. This research endeavor focused on elucidating the impacts of TKSO on colonic inflammatory responses and intestinal microbiota alterations in a murine model of colitis induced by dextran sulfate sodium (DSS), demonstrated that substantial supplementation with TKSO reduces the severity of colitis induced by DSS. Furthermore, TKSO effectively attenuated the abundance and expression of proinflammatory mediators while augmenting the expression of tight junction proteins in DSS-challenged mice. Beyond this, TKSO intervention modulated the intestinal microbial composition in DSS-induced colitis mice, specifically by enhancing the relative presence of Lactobacillus, Norank_f_Muribaculaceae, and Lachnospiraceae_NK4A136_group, while concurrently diminishing the abundance of Turicibacter. Additionally, an analysis of short-chain fatty acids (SCFAs) revealed noteworthy elevations in acetic, propionic, isobutyric, and butyric acids, and total SCFAs levels in TKSO-treated mice. In summary, these findings underscore the potential of TKSO to reduce the severity of colitis induced by DSS in mice through intricate modulation of the intestinal microbiota, metabolite profiles, and intestinal barrier repair, thereby presenting a promising avenue for the development of therapeutic strategies against intestinal inflammatory conditions. [ABSTRACT FROM AUTHOR]

Obesity has become one of the most serious chronic diseases threatening human health. Its onset and progression are closely related to the intestinal microbiota, as disruption of the intestinal flora promotes the production of endotoxins and induces an inflammatory response. This study aimed to investigate the variations in the physicochemical properties of various refined tea seed oils and their impact on intestinal microbiota disorders induced by a high-fat diet (HFD) through dietary intervention. In the present study, C57BL/6J mice on a HFD were randomly divided into three groups: HFD, T-TSO, and N-TSO. T-TSO and N-TSO mice were given traditionally refined and optimized tea seed oil for 12 weeks. The data revealed that tea seed oil obtained through degumming at 70 °C, deacidification at 50 °C, decolorization at 90 °C, and deodorization at 180 °C (at 0.06 MPa for 1 h) effectively removed impurities while minimizing the loss of active ingredients. Additionally, the optimized tea seed oil mitigated fat accumulation and inflammatory responses resulting from HFD, and reduced liver tissue damage in comparison to traditional refining methods. More importantly, N-TSO can serve as a dietary supplement to enhance the diversity and abundance of intestinal microbiota, increasing the presence of beneficial bacteria (norank_f__Muribaculaceae, Lactobacillus, and Bacteroides) while reducing pathogenic bacteria (Alistipes and Mucispirillum). Therefore, in HFD-induced obese C57BL/6J mice, N-TSO can better ameliorate obesity compared with a T-TSO diet, which is promising in alleviating HFD-induced intestinal microbiota disorders. [ABSTRACT FROM AUTHOR]

BACKGROUND: Cyclophosphamide (Cy) is a frequently used chemotherapeutic drug, but long‐term Cy treatment can cause immunosuppression and intestinal mucosal damage. The intestinal mucosal barrier and gut flora play important roles in regulating host metabolism, maintaining physiological functions and protecting immune homeostasis. Dysbiosis of the intestinal flora affects the development of the intestinal microenvironment, as well as the development of various external systemic diseases and metabolic syndrome. RESULTS: The present study investigated the influence of sciadonic acid (SA) on Cy‐induced immunosuppression in mice. The results showed that SA gavage significantly alleviated Cy‐induced immune damage by improving the immune system organ index, immune response and oxidative stress. Moreover, SA restored intestinal morphology, improved villus integrity and activated the nuclear factor κB signaling pathway, stimulated cytokine production, and reduced serum lipopolysaccharide (LPS) levels. Furthermore, gut microbiota analysis indicated that SA increased t beneficial bacteria (Alistipes, Lachnospiraceae_NK4A136_group, Rikenella and Odoribacter) and decreased pathogenic bacteria (norank‐f‐Oscillospiraceae, Ruminococcus and Desulfovibrio) to maintain intestinal homeostasis. CONCLUSION: The present study provided new insights into the SA regulation of intestinal flora to enhance immune responses. © 2024 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Objective: To investigate the potential beneficial effects of sciadonic acid (SA) on improving obesity induced by a high-fat diet in mice. Methods: Forty-eight male C57BL/6 mice were adaptively fed for one week and then randomly divided into the following groups: Control group (C), positive control group (S), model group (M), low-dose sciadonic acid group (LSA), medium-dose sciadonic acid group (MSA), and high-dose sciadonic acid group (HSA). The modeling process lasted for 16 weeks, and the low and high-dose groups were orally administered different doses of SA solution at a fixed time each day. After the modeling period, potential mechanisms of SA in regulating lipid metabolism in obese mice were explored, including aspects such as blood lipid metabolism, hepatic fat metabolism, hepatic oxidative stress, hepatic lipid synthesis, and expression of metabolism-related genes. Results: The high-dose SA intervention in obese mice significantly decreased the levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) in serum, while increasing high-density lipoprotein cholesterol (HDL-C) (P<0.05). It inhibited weight gain, reduced epididymal fat accumulation, and improved liver tissue damage. Additionally, SA significantly increased the activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mice (P<0.05), and significantly reduced the production of oxidative end products MDA (P<0.05), alleviated oxidative stress in vivo, and inhibited lipid synthesis by regulating the expression of genes related to lipid metabolism to improve lipid metabolism. Conclusion: SA could improve lipid metabolism disorders in obese mice by suppressing fat accumulation, alleviate oxidative stress, regulate lipid synthesis and metabolism. [ABSTRACT FROM AUTHOR]

Climate change has increased the overall impact of abiotic stress conditions such as drought, salinity, and extreme temperatures on plants. Abiotic stress adversely affects the growth, development, crop yield, and productivity of plants. When plants are subjected to various environmental stress conditions, the balance between the production of reactive oxygen species and its detoxification through antioxidant mechanisms is disturbed. The extent of disturbance depends on the severity, intensity, and duration of abiotic stress. The equilibrium between the production and elimination of reactive oxygen species is maintained due to both enzymatic and non-enzymatic antioxidative defense mechanisms. Non-enzymatic antioxidants include both lipid-soluble (α-tocopherol and β-carotene) and water-soluble (glutathione, ascorbate, etc.) antioxidants. Ascorbate peroxidase (APX), superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR) are major enzymatic antioxidants that are essential for ROS homeostasis. In this review, we intend to discuss various antioxidative defense approaches used to improve abiotic stress tolerance in plants and the mechanism of action of the genes or enzymes involved., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Mishra, Jiang, Chen, Paul, Chatterjee and Shen.)