curcumin uniformly reestablished closely associated relations among these genes
expression levels and decreased expression of genes characteristic of toxic
proinflammatory M1 microglia. It stimulated microglial migration to and phagocytosis of amyloid plaques both in-vivo and in ex vivo assays of sections of the
human AD brain and mouse brain. Curcumin also reduced levels of miR-155, a
micro-RNA reported driving a neurodegenerative microglial phenotype. Similarly,
it decreased CD33 and increased TREM2. Like curcumin, anti-Ab antibody
increased TREM2 in APPsw mice and decreased amyloid in human AD sections
ex vivo (Teter et al. 2019).
6.2.1.2 Resveratrol
Chemically resveratrol is (3,5,4′-trihydroxytrans-stilbene). Resveratrol is a stilbenoid polyphenol present in many nutritional foods and floras including red wine
grapevines, and peanuts. Like curcumin, resveratrol shows a broad range of pharmacological activities like anti-inflammatory, anticancer/proapoptotic, chemopreventive, antioxidant and antimicrobial (Malaguarnera 2019). Resveratrol actively
blocks inflammatory particles. The immunomodulatory actions of resveratrol
comprise the blocking of NF-jB in LPS, PMA or TNF-a-activated epithelial
(HeLa), macrophages, Jurkat, DCs and myeloid (U-937). Resveratrol block NF-jB
stimulation via blocking of IjB kinase (IKK) activity (Holmes-McNary and
Baldwin 2000). Resveratrol also blocks the expression of COX-2 and iNOS in
cytokines excited human primary small airway epithelial cells (HSAECs) although
it also blocks the transcription of COX-2 in HMECs via PMA stimulation.
Resveratrol also significantly blocks the release of TNF-a and NO in
LPS-stimulated N9 microglial and CMCs (Bi et al. 2005), the production of
PINFCs by splenic macrophages and also block lymphocytes (Kowalski et al.
2005). It also actively inhibits C5 anaphylatoxin (C5a)-activated inflammation
in-vivo. The secretion of INFCs in C5a-stimulated human and mouse neutrophils
block by the pre-incubation with resveratrol. Resveratrol also blocks
ERK-phosphorylation, production of glucuronide and C5a mediated oxidative
burst. Additionally, resveratrol blocks the production of INFCs and C5a-stimulated
neutrophil recruitment in the C5a-activated severe peritonitis mouse model (Issuree
et al. 2009). Resveratrol inhibits the expression of CAMs. It is also found that
resveratrol decrease IL-6-activated ICAM-1 appearance in ECs (Wung et al. 2005),
further to the blocking of Porphyromonas gingivalis LPS-activated endothelial
dysfunction in HMECs. Resveratrol also, block VCAM-1 and ICAM-1 appearance
on HMECs by inhibiting the NF-jB activation (Park et al. 2009). Resveratrol acts
by various cellular signaling pathways and shows anti‐inflammatory activity.
Resveratrol can potentiate its tumor-suppressive effect through modulation of the
signaling pathways of cellular components (fibroblasts, macrophages and T cells).
Also, studies have shown that resveratrol can suppress malignant phenotypes of
cancer cells acquired in response to stresses of the tumor microenvironment, such as
hypoxia, oxidative stress and inflammation (Han et al. 2019).
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expression levels and decreased expression of genes characteristic of toxic
proinflammatory M1 microglia. It stimulated microglial migration to and phagocytosis of amyloid plaques both in-vivo and in ex vivo assays of sections of the
human AD brain and mouse brain. Curcumin also reduced levels of miR-155, a
micro-RNA reported driving a neurodegenerative microglial phenotype. Similarly,
it decreased CD33 and increased TREM2. Like curcumin, anti-Ab antibody
increased TREM2 in APPsw mice and decreased amyloid in human AD sections
ex vivo (Teter et al. 2019).
6.2.1.2 Resveratrol
Chemically resveratrol is (3,5,4′-trihydroxytrans-stilbene). Resveratrol is a stilbenoid polyphenol present in many nutritional foods and floras including red wine
grapevines, and peanuts. Like curcumin, resveratrol shows a broad range of pharmacological activities like anti-inflammatory, anticancer/proapoptotic, chemopreventive, antioxidant and antimicrobial (Malaguarnera 2019). Resveratrol actively
blocks inflammatory particles. The immunomodulatory actions of resveratrol
comprise the blocking of NF-jB in LPS, PMA or TNF-a-activated epithelial
(HeLa), macrophages, Jurkat, DCs and myeloid (U-937). Resveratrol block NF-jB
stimulation via blocking of IjB kinase (IKK) activity (Holmes-McNary and
Baldwin 2000). Resveratrol also blocks the expression of COX-2 and iNOS in
cytokines excited human primary small airway epithelial cells (HSAECs) although
it also blocks the transcription of COX-2 in HMECs via PMA stimulation.
Resveratrol also significantly blocks the release of TNF-a and NO in
LPS-stimulated N9 microglial and CMCs (Bi et al. 2005), the production of
PINFCs by splenic macrophages and also block lymphocytes (Kowalski et al.
2005). It also actively inhibits C5 anaphylatoxin (C5a)-activated inflammation
in-vivo. The secretion of INFCs in C5a-stimulated human and mouse neutrophils
block by the pre-incubation with resveratrol. Resveratrol also blocks
ERK-phosphorylation, production of glucuronide and C5a mediated oxidative
burst. Additionally, resveratrol blocks the production of INFCs and C5a-stimulated
neutrophil recruitment in the C5a-activated severe peritonitis mouse model (Issuree
et al. 2009). Resveratrol inhibits the expression of CAMs. It is also found that
resveratrol decrease IL-6-activated ICAM-1 appearance in ECs (Wung et al. 2005),
further to the blocking of Porphyromonas gingivalis LPS-activated endothelial
dysfunction in HMECs. Resveratrol also, block VCAM-1 and ICAM-1 appearance
on HMECs by inhibiting the NF-jB activation (Park et al. 2009). Resveratrol acts
by various cellular signaling pathways and shows anti‐inflammatory activity.
Resveratrol can potentiate its tumor-suppressive effect through modulation of the
signaling pathways of cellular components (fibroblasts, macrophages and T cells).
Also, studies have shown that resveratrol can suppress malignant phenotypes of
cancer cells acquired in response to stresses of the tumor microenvironment, such as
hypoxia, oxidative stress and inflammation (Han et al. 2019).
216
V. K. Gurjar and D. Pal