Rheumatoid arthritis (RA) is a chronic, systemic, autoimmune disorder, predominantly symmetric, which causes joint inflammation, cartilage degeneration and bone erosion, resulting in deformity and the loss of physical function. Although the management of RA has steadily improved, the pathophysiological mechanism is incompletely elucidated, and therapeutic options are still limited. Due to shortcomings in the efficacy or safety profiles of conventional RA therapies, therapeutic alternatives have been considered. Therefore, natural extracts containing polyphenolic compounds can become promising adjuvant agents for RA global management, due to their antioxidant, anti-inflammatory and apoptotic properties. Polyphenols can regulate intracellular signaling pathways in RA and can generate different immune responses through some key factors (i.e., MAPK, interleukins (ILs 1 and 6), tumor necrosis factor (TNF), nuclear factor light k chain promoter of activated receptor (NF-κB), and c-Jun N-terminal kinases (JNK)). The critical function of the Toll like-receptor (TLR)-dependent mitogen-activating protein kinase (MAPK) signaling pathway in mediating the pathogenic characteristics of RA has been briefly discussed. Oxidative stress can trigger a change in transcription factors, which leads to the different expression of some genes involved in the inflammatory process. This review aims to provide a comprehensive perspective on the efficacy of polyphenols in mitigating RA by inhibiting signaling pathways, suggesting future research perspectives in order to validate their use.

No abstract

Background: Oxidative stress (OS) is a chief contributing factor in the pathological advancement of Schizophrenia (SCZ). In recent years, OS has emerged as an important aspect in the SCZ research and provides abundant opportunities and expectation for a better understanding of its pathophysiology, which may lead to novel treatment strategies. Introduction: The increased OS and formation of reactive oxygen species (ROS) leads to damage of cellular macromolecules. The excessive OS is associated with several physiological processes such as dysfunction of mitochondria and neuroglia, inflammation, underactive N-methyl-D-aspartate (NMDA) receptors and the abnormalities of fast-spiking gamma-aminobutyric acid (GABA) interneurons. Methods: The method adopted for the study are mainly based on the secondary search through a systemic literature review. The role of various anti-oxidants including vitamins are discussed in the reduction of SCZ. Results: Various preclinical and clinical evidence are also suggesting the involvement of OS and ROS in the progression of the disease. Recent human trials have shown that treatment with antioxidants to be effective in ameliorating symptoms and delaying the progression of SCZ pathology. The studies demonstrated that Innate and dietary antioxidants have shown beneficial effects by reducing the severity of positive symptoms (PS) and/or negative symptoms (NS) of SCZ. Conclusion: The present review critically evaluates the effect of antioxidants and highlights the role of OS in SCZ.

No abstract