Quercetin counteracts monosodium glutamate to mitigate immunosuppression in the thymus and spleen via redox-guided cellular signaling.

BACKGROUND: Chronic inflammation brought on by oxidative stress can result in several immunopathologies. Natural compounds with antioxidant characteristics, like quercetin, have shown effectiveness in reducing oxidative damage and regulating the immune response. PURPOSE: The commonly used food additive monosodium glutamate (M) causes immunosuppression by disrupting redox equilibrium and inducing oxidative stress. The goal of this work is to examine the therapeutic potential of quercetin against immunotoxicity brought on by M, revealing the molecular route implicated in such immunopathology by targeting the thymus and spleen, to support the development of future anti-inflammatory and antioxidant therapies. STUDY DESIGN AND METHODS: M-fed rats were employed as an immunotoxicity model and were supplemented with quercetin for four weeks. Hematological and biochemical parameters were measured; H&E staining, immunohistochemistry, flow cytometry, real-time quantitative PCR, and western blotting were performed. RESULTS: Based on the findings, TLR4 was activated by M to cause oxidative stress-mediated inflammation, which was alleviated by the supplementation of quercetin by modulating redox homeostasis to neutralize free radicals and suppress the inflammatory response. To prevent M-induced inflammation, quercetin demonstrated anti-inflammatory functions by blocking NF-kB activation, lowering the production of pro-inflammatory cytokines, and increasing the release of anti-inflammatory cytokines. By normalizing lipid profiles and lowering the potential risk of immunological deficiency caused by M, quercetin also improves lipid metabolism. Additionally, it has shown potential for modifying insulin levels, suggesting a possible function in controlling M-induced alteration in glucose metabolism. The addition of quercetin to M enhanced the immune response by improving immunoglobulin levels and CD4/CD8 expression in the thymus and spleen. Additionally, quercetin inhibited apoptosis by controlling mitochondrial caspase-mediated cellular signaling, suggesting that it may be able to halt cell death in M-fed rats. CONCLUSION: The results of this study first indicate that quercetin, via modulating redox-guided cellular signaling, has a promising role in reducing immune disturbances. This study illuminates the potential of quercetin as a safe, natural remedy for immunopathology caused by M, including thymic hypoplasia and/or splenomegaly, and paves the way for future anti-inflammatory and antioxidant supplements.

Effects of bamboo shoots (Bambusa balcooa) on thyroid hormone synthesizing regulatory elements at cellular and molecular levels in thyrocytes.

ETHNOPHARMACOLOGICAL RELEVANCE: Bamboo shoots (BS) are consumed in various forms and used largely in naturopathy for curing ailments since ancient times to present days. It is eaten in South East Asian countries in several indigenous preparations. In north east India, it is consumed predominantly and used as natural cure to treat various diseases. Although known for its beneficial effects, adverse effects including goitrogenic/antithyroidal potential are emerging. AIM OF THE STUDY: Endemic goiter exists in Manipur, India even after adequate iodine intake for consumption of BS. It is thus important to study the impact of this goitrogenic food on certain thyroid hormone synthesizing regulatory factors at cellular and molecular level in thyrocytes. MATERIALS AND METHODS: Phytochemical analysis of BS - Bambusa balcooa Roxb (BSBR) extract conducted. IC50 of the extract on thyrocytes in culture was determined. To study the antithyroid effects of this goitrogenic food, activity status of Na+-K+-ATPase, TPO and Deiodinase, mRNA and protein expressions of NIS, TPO and PAX8 were investigated with and without extra iodine in culture media. Simultaneously ROS generation in terms of H2O2 and antioxidant status, NO, LPO were assayed. RESULTS: Activities of the studied enzymes decreased depending on dose and time with increased H2O2, decreased antioxidants followed by increased NO with LPO. DNA damage and LDH also increased while mRNA and protein expression of NIS, TPO and PAX8 were downregulated. Extra iodine ameliorated all such effects partially. CONCLUSIONS: Bioactive constituents of the extract imbalances oxidative status of thyrocytes impairing action of hormone synthesizing elements at cellular and molecular level.