6.2.1.1 Curcumin
Curcumin is one of the natural diarylheptanoid belonging to the group of curcuminoids, which are natural phenols found in the rhizome of turmeric (Curcuma
longa) and other Curcuma species. The medicinal properties of curcumin used for
centuries in Ayurvedic medicine. Curcumin has a variety of therapeutic properties
like anti-proliferative, anti-cancer, pro-apoptotic, anti-angiogenic, antioxidant, etc.
It is one of the most reviewed and studied plant-derived bioactive molecules for its
immunomodulatory activity. Curcumin minimizes the inflammatory responses
(inflammation) by blocking nitric oxide (NO) production, (Surh et al. 2001)
COX-2, iNOS, NK-kB, inducible and LOX in IFN-c and NK cells or
TNF-a-stimulated macrophages. In PMA and hydrogen peroxide activated
human acute myeloid leukemia cell lines, curcumin blocked NF-jB stimulation via
inhibition of breakdown and phosphorylation of I kappa B alpha (IjB-a). The PKC,
which controls the production and survival of the cell, is stimulated by PMA.
Furthermore, lipopolysaccharide (LPS) and TNF-a also stimulate PKC, which then
stimulates NF-jB (Holden et al. 2008). Hence, curcumin might lessen NF-kB
stimulation by the blocking of PKC. The anti-inflammatory property of curcumin
moderately facilitated by preventing the activator protein-1 (AP-1) and NF-jB. The
AP-1 and NF-jB act together and may increase tumor growth. Curcumin lessened
the binding of NF-jB and AP-1 on the treatment of glioma cells (Dhandapani et al.
2007). The AP-1-stimulation also blocked by curcumin in TNF- a-stimulated
bovine aortic endothelial cells (BAOECs).
The stimulated ICs to produce PINFLCs that play an important role in various
inflammation diseases. The expression of PINFLCs like IL-1, IL-6, IL-12 and
TNF-a, blocked by curcumin via LPS or PMA-activated macrophages, monocytes,
splenic lymphocytes and DCs (Gao et al. 2004; Kim et al. 2005). The binding of T
cells to endothelial and APCs is dependent on CAMs. The binding of monocytes to
endothelial cells inhibited by pre-treatment with curcumin. Furthermore, the
appearance of ICAM-1, VCAM-1 and ELAM-1 also reduced in TNF-a-activated
HUVECs via blocking of NF-jB (Kumar et al. 1998). Curcumin improved the
RANKL-mediated differentiation, fusion and development of osteoclasts and has an
immunomodulatory result on macrophage polarization. The defensive action of
curcumin on osteoclast genesis facilitated by decreasing the up-regulation of Akt
and p65 phosphorylation and the stimulation of the downstream transcription factor
NFATc1 (Yang et al. 2020). Curcumin treatment reduced activation of the NFkB,
MAPK, AKT and pBAD pathways either systemically, or within the inflamed
kidneys (Wu et al. 2020). Curcumin is capable of emulating anti-Ab vaccine in
stimulating phagocytic clearance of amyloid by decreasing CD33 and increasing
TREM2 and transmembrane immune signaling adaptor (TyroBP) though improving
neuroinflammatory systems concerned in neurodegenerative diseases. A low dose
of curcumin decreased CD33 (Siglec-3) and increased triggering receptor expressed
on myeloid cells 2 (TREM2) expression and also increased TyroBP, which controls
a neuroinflammatory gene network implicated in AD, in addition to phagocytosis
markers cluster of differentiation 68 (CD68) and Arginase 1. A low dose of
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215
Curcumin is one of the natural diarylheptanoid belonging to the group of curcuminoids, which are natural phenols found in the rhizome of turmeric (Curcuma
longa) and other Curcuma species. The medicinal properties of curcumin used for
centuries in Ayurvedic medicine. Curcumin has a variety of therapeutic properties
like anti-proliferative, anti-cancer, pro-apoptotic, anti-angiogenic, antioxidant, etc.
It is one of the most reviewed and studied plant-derived bioactive molecules for its
immunomodulatory activity. Curcumin minimizes the inflammatory responses
(inflammation) by blocking nitric oxide (NO) production, (Surh et al. 2001)
COX-2, iNOS, NK-kB, inducible and LOX in IFN-c and NK cells or
TNF-a-stimulated macrophages. In PMA and hydrogen peroxide activated
human acute myeloid leukemia cell lines, curcumin blocked NF-jB stimulation via
inhibition of breakdown and phosphorylation of I kappa B alpha (IjB-a). The PKC,
which controls the production and survival of the cell, is stimulated by PMA.
Furthermore, lipopolysaccharide (LPS) and TNF-a also stimulate PKC, which then
stimulates NF-jB (Holden et al. 2008). Hence, curcumin might lessen NF-kB
stimulation by the blocking of PKC. The anti-inflammatory property of curcumin
moderately facilitated by preventing the activator protein-1 (AP-1) and NF-jB. The
AP-1 and NF-jB act together and may increase tumor growth. Curcumin lessened
the binding of NF-jB and AP-1 on the treatment of glioma cells (Dhandapani et al.
2007). The AP-1-stimulation also blocked by curcumin in TNF- a-stimulated
bovine aortic endothelial cells (BAOECs).
The stimulated ICs to produce PINFLCs that play an important role in various
inflammation diseases. The expression of PINFLCs like IL-1, IL-6, IL-12 and
TNF-a, blocked by curcumin via LPS or PMA-activated macrophages, monocytes,
splenic lymphocytes and DCs (Gao et al. 2004; Kim et al. 2005). The binding of T
cells to endothelial and APCs is dependent on CAMs. The binding of monocytes to
endothelial cells inhibited by pre-treatment with curcumin. Furthermore, the
appearance of ICAM-1, VCAM-1 and ELAM-1 also reduced in TNF-a-activated
HUVECs via blocking of NF-jB (Kumar et al. 1998). Curcumin improved the
RANKL-mediated differentiation, fusion and development of osteoclasts and has an
immunomodulatory result on macrophage polarization. The defensive action of
curcumin on osteoclast genesis facilitated by decreasing the up-regulation of Akt
and p65 phosphorylation and the stimulation of the downstream transcription factor
NFATc1 (Yang et al. 2020). Curcumin treatment reduced activation of the NFkB,
MAPK, AKT and pBAD pathways either systemically, or within the inflamed
kidneys (Wu et al. 2020). Curcumin is capable of emulating anti-Ab vaccine in
stimulating phagocytic clearance of amyloid by decreasing CD33 and increasing
TREM2 and transmembrane immune signaling adaptor (TyroBP) though improving
neuroinflammatory systems concerned in neurodegenerative diseases. A low dose
of curcumin decreased CD33 (Siglec-3) and increased triggering receptor expressed
on myeloid cells 2 (TREM2) expression and also increased TyroBP, which controls
a neuroinflammatory gene network implicated in AD, in addition to phagocytosis
markers cluster of differentiation 68 (CD68) and Arginase 1. A low dose of
6 Natural Compounds Extracted from Medicinal Plants …
215