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Sesamum oil

Sesame oil extracted from Sesamum indicum has been used in various
Asian traditional medicines to lighten pain in inflammatory conditions of the various
tissues such as joints, teeth, skin (D.-Z. C. Hsu, S.-J.; Chu, P.-Y.;
Liu, M.-Y. , 2013, ).

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A rat model of adjuvant induced arthritis, SO was tested and was
capable of reducing the biochemical consequences of oxidative stress: lower
plasmatic levels of thiobarbituric acid reactive substances and reduced
gamma-glutamyltransferase activity in the joints (Sotnikova, 2009, ). In a rat model of acute arthritis, SO strongly hindered the
inflammatory reaction, thinning the inflammatory infiltrate, lowering the
levels of inflammatory mediators, hindering the activity of NF-kB within the
mast cells and activation of complement system (D.-Z. C. Hsu, S.-J.; Chu, P.-Y.;
Liu, M.-Y. , 2013, ). In another rat model of OA, SO alleviated joint pain by
inhibiting oxidative aggression via falling the levels of lipids peroxidation,
production of superoxide anion and peroxynitrite in the muscles associated with
nuclear factor erythroid-2-related factor (D.-Z. C. Hsu, P.-Y.; Jou, I.-M. ,
2016, ). SO
is active in experimentally induced arthritis through its minor constituents which
without it is inactive, decreasing the clinically visible joint inflammation, in
addition to its serum markers including oxidative stress related molecules, RA
markers, inflammatory eicosanoids and cytokines and the activity of hydrolytic enzymes;
additionally, bone loss was also diminished (Yadav, 2016, ).

In a study on knee OA patients, orally administrated sesame compared
to standard therapy produced better outcomes in terms of objective and
subjective manifestations in comparison to standard therapy alone (Eftekhar Sadat, 2013, ). In patients with knee OA, a placebo trial on sesame seed management
was associated with a noticed drop in serum levels of malondialdehyde and of
high-sensitivity C-reactive protein (hs-CRP) after two months of treatment and
significantly lowered levels of IL-6 after treatment (Khadem Haghighian, 2015,).

The ability of SI to protect from the forward consequences of inflammation
and oxidative stress is being due to presence the lignans. It contains sesamin
and its hydroxylated counterpart, sesamolin. Similar biological activity has a
phenolic compound, sesamol (3,4-methylene-dioxy-phenol) which results from the
degradation of sesamolin (Yashaswini, 2017, ). Sesamol has been proven to alleviate joint inflammation,
cartilage degradation, and periarticular bone resorbtion in adjuvant-induced
arthritis animal model. This action was paralleled by a drop in the level of
pro-inflammatory cytokines and in the activity of tissue-destructive enzymes (Hemshekhar, 2013,).

In addition, restorations of the oxidant homeostasis reflected in
decreased oxidative stress markers and a boost in the activity of protective
enzymes were noticed. The hydroperoxides-scavenging capacity of sesamol makes
it able to arrest the oxidation state of iron and consequently the conversion
of inactive LOX (Fe2+) to active LOX (Fe3+), which leads to the inhibition of
this inflammation-promoting enzyme (Yashaswini, 2017, ).

 

 

Whitania somnifera

Withania somnifera (WS) which
also entitled ashwagandha, is a powerful anti-osteoarthritic and
anti-inflammatory plant (N. B. Singh, M.; de Jager, P.;
Gilca, M. , 2011).

WS extract was in vitro studied and it was noticed to
inhibit liposaccharide S induced synthesis of pro-inflammatory cytokines
(TNF-alpha, IL-1beta and IL-12) in peripheral and synovial fluid mononuclear
cells from rheumatoid arthritis subjects in vitro, but had no effect on IL-6 synthesis
(D. A. Singh, A.; Maurya, R.; Naik,
S. , 2007,).

The WS extract also showed inhibitory effects on collagenase
activity against the degradation of the bovine type I collagen of tendon
Achilles, that may be useful in joint disease treatment (Ganesan, 2011).

In experimental rats induced arthritis model, WS root powder had
shielding effect on bone collagen (Rasool, 2007).

The aqueous extract of WS produced significant reduction of scores
for pain, stiffness and disability in patient subjects with knee joint inflammation
in a randomized, double blind placebo study (Ramakanth, 2016).

Withaferin A, belonging to
the steroid class of phytochemicals, is thought to be one of contributor
compounds to the beneficial effects of WS in OA subjects (D. A. Singh, A.; Maurya, R.; Naik,
S. , 2007,). Withaferin
A suppresses NF-kB activation by targeting a crucial cysteine 179 in I_B
kinase _, and by inhibition of the NF-kB Essential Modulator/ I_B kinase _
association complex formation, according to molecular docking and molecular dynamics
simulations studies (Grover, 2010,; Heyninck, 2014,).

 

Neutraceuticals target the NF-kB pathway in arthritis

 

Camel milk

Camel milk revealed a
various anti-inflammatory effect via downregulation of TNF-?, COX-2,
iNOS and its upstream effector NF-?B together with enhancing the IL-10
anti-inflammatory pathway. These anti-inflammatory mechanisms are described
additionally in further studies which reported that camel milk posses marked anti-inflammatory
actions in experimental models (Darwish HA, 2012;), (Zhu WW, 2016), (Rosillo MA, 2014). The master anti-inflammatory component of camel milk is the
lactoferrin protein which has been characterized to manage TNF-?, IL-1 and IL-6
in mononuclear cells in vitro and in vivo in response to LPS
stimulation. Lactoferrin has been also reported to enhance the levels of IL-10
in a rat model of inflammation (Legrand D, 2005;). The observed downregulation of activated NF-?B p65 in pouch
lining confirms the effectual anti-inflammatory performance of camel milk (Ebaid H, 2015). Meanwhile, the observed downregulation of TNF-?, COX-2 and iNOS
in arthritic rats is prone to the inhibition of their upstream NF-?B
transcription factor (Phillips DC, 2010), (Rosillo MA, 2014).

 

Glucosamine

Glucosamine is a building unit of long chain glycosaminoglycans correlated
to a protein in proteoglycan molecules called aggrecans forming a component of
the cartilage matrix. When given exogenously, glucosamine exerts specific
effects on cartilage and chondrocytes in osteoarthritis (Rovati LC, 2012). Glucosamine affects gene expression of arthritic cartilage, and its
therapeutic effects are linked to its anti-catabolic activities (Reginster JY, 2012). Glucosamine is given in vitro to reduce prostaglandin E2 (PGE2)
production and inactivation of the nuclear factor kappa B (NF-jB) pathway, thus
inhibiting the cytokine intracellular signalling cascade in chondrocytes and
synovial cells . In OA, glucosamine induces reversal of the pro-inflammatory
and joint-degenerating effects of interleukin-1 (IL-1) (Rovati LC, 2012). Interleukin-1 beta (IL-1b) is a potent pro-inflammatory cytokine
produced in high amounts in the OA joint, where it triggers the expression of
inflammatory factors such as cyclooxygenase-2 (COX-2), inducible form of nitric
oxide (iNOS), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNFa).
IL-1b also induces cells to produce moreIL-1b as well as matrix degradation
factors, such as metalloproteinases (MMPs) and a disintegrin and
metalloproteinase with a thrombospondin type 1 motif, member TSs (ADAMTSs).

Most of these genes are under the transcriptional control of NF-kB.
Glucosamine at a appropriate concentrations lessens COX-2, iNOS, and microsomal
prostaglandin Esynthase-1 (mPGEs1) gene expression and PGE2 synthesis after
IL-1b stimulation, suggesting that glucosamine can control the cascade
triggered by inflammatory stimuli (Chan PS, 2005;).

 

Transcription of IL-6,
IL-8, IL-24 and TNF-? genes is controlled by multiple transcription factors,
such as NF-?B (H. J. Ju Y, Sakamoto K, Ogawa H, Nagaoka I. , 2008; ; Liu H, 2000; ). Attractively, the functions of NF-?B are controlled
by OGlcNAc modification (Li Y, 2014) (Ramakrishnan P, 2013;). Furthermore, GlcN inhibits the TNF-?-induced chemokines
expression by rat smooth muscle cells via the O-GlcNAc modification of
NF-?B p65 (Xing D, 2011).

Moreover, it`s previously
revealed that GlcN inhibits the expression of chemokine and adhesion molecule
by endothelial cells via O-GlcNAc modification of NF-?B p65  (H. J. Ju Y, Sakamato K, Ogawa H, Nagaoka I., 2008). GlcN had been confirmed to enhance the O-GlcNAc
modification of NF-?B p65 but suppresses the expression of cytokines in MH7A
cells. These observations likely suggest that theexpression of proinflammatory
cytokine genes may be regulated by the mechanism involving the O-GlcNAc-modification
of NF-?B.

 

Chondroitin and glucosamine combination

Mixture of glucosamine and chondroitin sulphate restrained
IL-1-induced gene expression of iNOS, COX- 2, m PGEs, and NF-?B in inflamed
cartilage which lead to decreased NO and PGE2 production, which are being mediators
responsible for the chondrocytes cell death and inflammatory reactions (J. P. C. Chan P. S. , and M. W.
Orth, , 2006.; J. P. C. Chan P. S. , G. J. Rosa, and M. W. Orth, “, 2005). Different ways glucosamine or chondroitin sulphate could reduce
synthesis of the COX-2 enzyme. One way is the inhibition of the IL-1 beta
induced NF-?B pathway by glucosamine results in reduced synthesis of the
COX-2 enzyme (Largo R. , 2003) (Gouze JN, 2002;). A further way in which glucosamine inhibits COX-2 activity is
the prevention of COX-2 translational N-glycosylation and the facilitation of
COX-2 protein turnover (Jang B. C. , 2007). Chondroitin alone reduces the nuclear translocation of NF-?B,
which lessen the formation of proinflammatory cytokines IL- 1beta and TNF-alpha
and enzymes such as cyclooxygenase 2 (COX-2) and nitric oxide synthase-2
(NOS-2) (du Souich P. , 2009).

The anti-inflammatory capability of CS was also tested in a rabbit
atherosclerosis model, where, CS reduced the proinflammatory molecules
C-reactive protein and IL-6 and the expression of MCP-1 and COX-2 in the
peripheral blood mononuclear cells as well. It also inhibited NF-?B that
is responsible for the induction of inflammatory processes (Herrero-Beaumont G., 2008).

Additionally, inflammation mediators activate various cartilage
degenerating enzymes. The mRNA expression of such enzymes (MMP-13 and
aggrecanases (ADAMTS-5) was reduced in cartilage explants incubated with GlcN·S and CS. In the same study, the tissue inhibitor of
metalloproteinase- 3 (TIMP-3), a potent inhibitor of ADAMTS, was upregulated.
Glucosamine alone was shown to inhibit the activation process of MMP-2 and MMP-
9 expression, via down regulation of the NF-?B pathway (Rajapakse N. , 2007).

Mediators of Inflammation are responsible for narrowed
biosynthesis of cartilage material. In rat chondrocytes models have shown that
IL-1? inhibits the expression of the key enzyme in the biosynthesis of
cartilage GAG chains and a dose dependently glucosamine was able to reduce this
inhibition (Gouze J. N. , 2001).

 

Omega 3

Omega-3 polyunsaturated fatty acids, such as linolenic acid and
eicosapentaenoic acid, which are found in plant and fish oils (Thiyagarajan P, 2011. ). They are known for their anti-inflammatory action, which has
been shown in several studies. They have been successfully used in clinical
trials, mainly to treat rheumatoid arthritis. In vitro studies showed
that omega-3 fatty acids enhance collagen synthesis and reduce the inflammatory
mediator PGE2 (Hankenson K. D.  & Allen, 2000). EPA, when being oxygenated, results in the bioactive product
resolving E1 (RvE1). By activation of a specific receptor, ChemR23, RvE1
considerably lessens inflammatory processes via inhibiting the NF-?B
pathway that is mediator for many of these processes. Omega-3 fatty acids
decrease IL-1-induced aggrecanase and collagenase activity and reduce mRNA
expression of ADAMTS-4, COX-2, IL-1?, and TNF-?. Furthermore,
they decrease the protein levels of several MMPs (Curtis C. L. , 2002).

 Conclusion

 

    Altogether, since
dysregulated NF-?B activation is implicated in various inflammatory diseases,
targeting the NF-?B signalling pathway represents an attractive approach for
anti-inflammatory trials in rheumatoid arthritis. It`s noticed that use of nutrients
in rheumatology is atypical and eventually, The enhanced interest of RA
patients in nutrient approach is a reality; hence rheumatologists should advice
their patients with scientific tools and the best evidence available. In this
sense the anti-arthritic ability of nutrients sets its position which supports precise
scientific evaluation on all approaches that improve the treatment of rheumatic
diseases. Present the nutrient approaches that possibly advantageous for RA
patients, even though there is still a long way ahead in terms of research in
order to draw firm conclusions. There are no long-lasting studies, nor studies
to assess series of joint damage; conversely some complementary therapies may signify
a prospect to build up the quality of our patient`s life, may be along with
integrated management of RA patients in the future.

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