## 4 Discussion
This study showed the significant inhibition of all inflammatory cytokines in the serum of AIA rats that received walnut, peanut, cashew, and hazelnut oil. The biggest effect was seen with the walnut and peanuts oil diets. Nuts exert a potent anti-inflammatory effect due to the high content in many macro- and micro-nutrients including \(\omega\)-3 PUFAs, oleic acid, dietary fibers, magnesium, L-arginine, vitamins, and polyphenols (phytosterols and phenolic compounds) [17]. Therefore, it seems reasonable to say that the protective effect of all these nuts oils on the AIA group is due to their anti-inflammatory potential. In cohort studies, the regular daily serving and consumption of different types of nuts are allied with reduced coronary heart disease (CHD), diabetes, cardio-metabolic risk, the majority of cancers, and mortality rates possibly due to their antioxidant and anti-inflammatory properties [60; 61; 62]. Similarly, a cross-sectional study by [PERSON] et al. [27] investigating the connotation between nuts and systemic inflammation in a multiethnic population demonstrated that regular nut intake was inversely proportional to blood levels of CRP, IL-6, and fibrinogen. The maximum improvement in RA severity was noticed with walnut, which could be related to its effect on inflammatory mediators. The effects of EPA and DHA on inflammation and immunity were consistent with the existing mechanisms of fatty acid action. The highly unsaturated nature of EPA and DHA have discernible effects on membrane order in immune cells [63]. DHA and EPA are incorporated into inflammatory and immune cells at the expense of ARA acid [64], reducing the substrate quantity available to produce inflammatory and immunoregulatory eicosanoid [65; 66]. \(\omega\)-3 fatty acids can modify the production of eicosanoids and cytokines and the expression of key cell surface proteins [67]. The \(\omega\)-3 PUFAs compete with \(\omega\)-6 ARA, thus reducing the production of lipid-derived pro-inflammatory compounds. In addition, the anti-inflammatory action exerted by EPA and DHA is mediated by a decrease in the expression of adhesion molecules both on immune cells and on endothelium [12]. Dietary fat composition affects the fatty acid composition of inflammation and immune cells. These cells contain different compositions of PUFAs that can readily change, providing a link between inflammation and immunity and dietary PUFAs intake [68]. Fish oil supplementation leads to a partial replacement of ARA in cell membranes by EPA. This in turn decreases the production of ARA-derived mediators [68]. Our data are consistent with a previous study [69] that revealed that the levels of pro-inflammatory cytokines decreased with increasing dietary components from \(\omega\)-3. The observed significant differences were the reductions in CRP, IL-6, and TNF-\(\alpha\). The study findings also agreed with [PERSON] et al. [70], who stated that a high dose of \(\alpha\)-linolenic acid decreased IL-1 and TNF-\(\alpha\) production by monocytes cells. Adding linseed oil with a high content of ALA to a low-fat diet caused a significant reduction in lymphocyte proliferation, but circulating antibody levels were unaffected [71]. The majority of nuts contain MUFAs as the dominant FAs. However, walnuts are very rich in \(\omega\)-3 PUFAs (13-18 g/1 oz or 6.9-17.6%) [72; 73]. Such high levels of \(\omega\)-3 PUFAs could explain the inhibitory effect of walnut oil on the levels of RF and all of the measured inflammatory cytokines in AIA-treated rats in this study. Supporting this, the inhibitory effect of \(\omega\)-3 PUFAs against RA is well-reported in the literature.