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Osteoarthritis
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Curcumin is the main bioactive anti-inflammatory polyphenol in the plant rhizome turmeric. In cell studies, curcumin has the ability to block several inflammatory mediators. In vitro curcumin can inhibit NF-κB and COX-2, and chondrocyte studies show an ability to block the expression of MMP. There have been several clinical studies published showing some effectiveness for use of curcumin in OA. In one study, over a period of 4 weeks, patients with OA received a daily dose of 2 g of curcumin in comparison to patients given the NSAID, ibuprofen. After 4 weeks, there was no difference in pain score or function score between the two groups, leading to the conclusion that turmeric is as effective as ibuprofen for OA (Kuptniratsaikul et al., 2014). Other studies also show reduction in patient reports of pain as well as reduction of inflammatory markers with lower doses of curcumin, 200 mg, for 3 months or 8 months (Belcaro et al., 2010a; Belcaro et al., 2010b).
AI and Chronic Inflammation
Published in Louis J. Catania, AI for Immunology, 2021
Finally, the clinical course of chronic inflammation distinguishing it from acute inflammation, beyond duration, is the magnitude of its pathological consequences on the body at large. According to most medical experts, chronic inflammatory disease is the progenitor or originating cause of all the major human disease categories (Figure 3.2). The clinical basis for this thesis lies in the diffuse and destructive nature of the chronic inflammatory process. As opposed to the acute inflammatory reaction, being a localized tissue process, in chronic inflammation the persistent inflammatory mediators and cellular components damage tissue locally (e.g., psoriasis, arthritis), in specific organ systems (e.g., Crohn’s disease, glomerulonephritis), or throughout the body (e.g., vasculitis, diabetes and COVID-19 – more in Chapter 5).
Fibromyalgia
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
A variety of possible mechanisms have been proposed but, because these mechanistic abnormalities are not found in all patients, finding effective treatments has been difficult (Table 7.1). There is increasing evidence that changes in inflammatory mediators and a disturbed balance of pro- and anti-inflammatory cytokines can occur. Fibromyalgia has also been considered a stress-related disorder with dysfunction of the hypothalamic pituitary adrenocortical (HPA) axis. Some researchers have shown increases in oxidative stress and toxic metabolites of lipid peroxidation, while others have studied the idea that fibromyalgia could be a sympathetically maintained neuropathic pain syndrome. It has also been proposed that dorsal root ganglia and peripheral sensory neuron sodium channels may play a major role in fibromyalgia pain transmission.5
Mechanisms of action of vitamin B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin) in pain: a narrative review
Published in Nutritional Neuroscience, 2023
A. M. Paez-Hurtado, C. A. Calderon-Ospina, M. O. Nava-Mesa
Pain is a serious and widespread public health problem affecting around 10%–20% of adults worldwide [1–5]. There are three different types of pain subcategorized according to their pathophysiological mechanisms by the International Association for the Study of Pain. Nociceptive pain is a pain sensation caused by ‘an actual or threatened damage to non-neural tissue and is due to activation of nociceptors’ [6]. Pain initiated or caused by a lesion or a disease of the somatosensory system is referred to as neuropathic pain. Nociplastic pain is defined as ‘pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain’ [6]. Inflammatory pain is a type of nociceptive pain which results from hypersensibility of nociceptors by inflammatory mediators [7].
Streptozotocin mechanisms and its role in rodent models for Alzheimer’s disease
Published in Toxin Reviews, 2023
Mazzura Wan Chik, Nur Adiilah Ramli, Nurul Aqmar Mohamad Nor Hazalin, Gurmeet Kaur Surindar Singh
Neuroinflammation in AD results from the accumulation of Aβ and tau protein. The development of neuroinflammation is usually seen in the group treated with STZ because of its NO donor and ROS generator properties, which cause neuronal damage ( Weinstock and Shoham, 2004, Chen et al.2013). Thus, the inflammatory-mediated pathway is activated to repair the neuronal damage with the help of microglia and astrocytes via phagocytosis (Phatnani and Maniatis 2015). The inflammatory mediator (cytokine) is released at the site of injury to regulate and intensify the extent of the immunoreaction. Prolonged activation of microglia reduces their ability to clear Aβ, since prolonged periods of Aβ production cause their enlargement and dysfunction. This leads to the activation of more microglia and the eventual exacerbation of the neuroinflammation because the clearance of Aβ by microglia will release proinflammatory cytokines tumor necrosis factor (TNF), interleukin 6 (IL-6) and interleukin 1B (IL-1B) and ROS and promote an accumulation of Aβ that contributes to neurodegeneration (Hickman et al. 2008) as shown in Figure 3. Postmortem brain sections revealed clusters of activated microglia and astrocytes around the Aβ plaques and tau tangles (Navarro et al. 2018).
The effect of ARVs on the MEKKK1 gene promoter, inflammatory cytokine expression and signalling in acute treated Jurkat T cells
Published in Xenobiotica, 2022
Avril Kirsten Moses, Terisha Ghazi, Savania Nagiah, Anil Chuturgoon
Inflammation is a normal process if regulated; however dysregulation can result in permanent tissue damage and lead to acute and chronic inflammation (Liu et al. 2017). Inflammation occurs in response to a stimulus, causing swelling, heat, pain and redness, eventually leading to the recruitment of immune cells, and the release of additional inflammatory mediators (Khalaf et al. 2010; Sandler and Sereti 2014). Cytokines, primarily produced by T-lymphocytes (T-cells) and macrophages, make up one class of inflammatory biomarkers and are the chief mediators of inflammatory responses, with either pro-inflammatory or anti-inflammatory abilities (Brenner et al. 2014). Elevated levels of pro-inflammatory cytokines, for example, tumour necrosis factor (TNF) and interleukin-6 (IL-6) have been linked to diseases, which include pulmonary and cystic fibrosis, and may be elevated in AIDS (Zhang and An 2007; Khalaf et al. 2010).