“…In previous studies, we found that the main components of AFPR are hexadecenoic acid, hexadecanoic acid, E-Octadecenoic acid, etc., and have anti-inflammatory bone loss, anti-cancer, anti-pruritus, antidepression, anti-fatigue, and other effects. [5][6][7][8][9] We have demonstrated that AFPR can improve depression through neuroinflammation in our previous studies, but its mechanism of action to improve depression through neuroinflammation has not been clarified. Studies have shown that xiaoyao pills can improve depression by inhibiting lipopolysaccharide-induced inflammatory responses.…”
Purpose
Neuroinflammation is a significant etiological factor in the development of depression. Traditional Chinese medicine (TCM) has demonstrated notable efficacy in the treatment of inflammation. Our previous study surfaces that the active fraction of
Polyrhachis vicina
Roger (AFPR) has antidepressant and anti-neuroinflammatory effects, but the specific mechanisms remain to be elucidated. The objective of this study was to examine the impact of AFPR on inflammation in depression via the FTO/miR-221-3p/SOCS1 axis.
Methods
Chronic unpredictable stress (CUMS)-induced rats and LPS-induced BV2 cells were employed to simulate depression models in vivo and in vitro. The levels of inflammatory factors were detected using the ELISA assay. The expression of genes and proteins was detected using qRT-PCR and Western blot. Gene interactions were detected using the dual luciferase reporter gene. Protein-RNA interactions were investigated using RNA methylation immunoprecipitation (MeRIP) and RNA immunoprecipitation (RIP). Neuroinflammation in the brain was examined through H&E staining, while neuronal apoptosis was assessed using TUNEL staining.
Results
The results showed that AFPR ameliorated depression induced inflammation by increasing SOCS1 expression. However, SOCS1 was identified as a target of miR-221-3p. Overexpression of miR-221-3p decreased the expression of SOCS1 and increased the levels of NF-κB, IL-7, and IL-6. In addition, we found that miR-221-3p was regulated by FTO-mediated m6A modification through MeRIP and RIP experiments. Interference with miR-221-3p and overexpression of FTO resulted in increased SOCS1 gene expression and decreased levels of NF-κB, IL-7, and IL-6, which were reversed by AFPR.
Conclusion
AFPR inhibits the maturation of pri-miR-221-3p through FTO-mediated m6A modification, reduces the production of miR-221-3p, increases the expression of SOCS1, and reduces the level of inflammation, thereby improving depressive symptoms.
“…In previous studies, we found that the main components of AFPR are hexadecenoic acid, hexadecanoic acid, E-Octadecenoic acid, etc., and have anti-inflammatory bone loss, anti-cancer, anti-pruritus, antidepression, anti-fatigue, and other effects. [5][6][7][8][9] We have demonstrated that AFPR can improve depression through neuroinflammation in our previous studies, but its mechanism of action to improve depression through neuroinflammation has not been clarified. Studies have shown that xiaoyao pills can improve depression by inhibiting lipopolysaccharide-induced inflammatory responses.…”
Purpose
Neuroinflammation is a significant etiological factor in the development of depression. Traditional Chinese medicine (TCM) has demonstrated notable efficacy in the treatment of inflammation. Our previous study surfaces that the active fraction of
Polyrhachis vicina
Roger (AFPR) has antidepressant and anti-neuroinflammatory effects, but the specific mechanisms remain to be elucidated. The objective of this study was to examine the impact of AFPR on inflammation in depression via the FTO/miR-221-3p/SOCS1 axis.
Methods
Chronic unpredictable stress (CUMS)-induced rats and LPS-induced BV2 cells were employed to simulate depression models in vivo and in vitro. The levels of inflammatory factors were detected using the ELISA assay. The expression of genes and proteins was detected using qRT-PCR and Western blot. Gene interactions were detected using the dual luciferase reporter gene. Protein-RNA interactions were investigated using RNA methylation immunoprecipitation (MeRIP) and RNA immunoprecipitation (RIP). Neuroinflammation in the brain was examined through H&E staining, while neuronal apoptosis was assessed using TUNEL staining.
Results
The results showed that AFPR ameliorated depression induced inflammation by increasing SOCS1 expression. However, SOCS1 was identified as a target of miR-221-3p. Overexpression of miR-221-3p decreased the expression of SOCS1 and increased the levels of NF-κB, IL-7, and IL-6. In addition, we found that miR-221-3p was regulated by FTO-mediated m6A modification through MeRIP and RIP experiments. Interference with miR-221-3p and overexpression of FTO resulted in increased SOCS1 gene expression and decreased levels of NF-κB, IL-7, and IL-6, which were reversed by AFPR.
Conclusion
AFPR inhibits the maturation of pri-miR-221-3p through FTO-mediated m6A modification, reduces the production of miR-221-3p, increases the expression of SOCS1, and reduces the level of inflammation, thereby improving depressive symptoms.
“…The food, pharmaceutical, and textile industries generate toxic effluents derived from the dyeing procedure with azo dyes, which are resistant to degradation by light and microorganisms and are not removed by conventional treatment systems (Chequer et al., 2011). Therefore, the azo dyes used for these industries may affect the integrity of the ecosystem by producing toxic, genotoxic, mutagenic, carcinogenic, and lethal effects for aquatic and terrestrial organisms and affect water resources and soil integrity (Li et al., 2022; Motta et al., 2019; Puvaneswari et al., 2006; Wu et al., 2021). Notably, the different azo dyes for each industry are regulated for use, but all industries generate toxic effluents that represent a planetary health concern (Chequer et al., 2011).…”
The food industry uses dyes mainly to overcome color loss during the processing and storage of products, with the azo dyes currently being the most employed. Studies on the safety of using these dyes in foods started in the 1950s and have indicated the potential for concern. This review discusses the risk assessment of food intake containing artificial azo dyes. There are case reports and, subsequently, double‐blind placebo‐controlled trials in some individuals who may experience adverse effects from the intake of azo dyes, but it is unclear whether these adverse effects are restricted to specific populations or more generalized. In view of this, different toxicological endpoints are evaluated to verify toxic effects in in vitro and in vivo models and to establish the no observed adverse effect level. Exposure estimation studies have shown that human exposure to azo dyes via oral intake is mainly below the acceptable daily intake established by advisory bodies. However, most countries do not have studies that estimate the oral intake of azo dyes. In this case, local food diversity and racial–ethnic specificities are not considered when stating the exposure estimate is below the acceptable daily intake for the human population and thus may not represent actual intake. Concerning the scenario established above, this review discusses the most critical gaps to be overcome to contribute to the direction of future studies and the development of more effective public policies concerning the safety of the intake of artificial azo dyes.
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