The methanolic crude extract from the leaves of Acanthus ilicifolius (Holly mangrove, sea holly) inhibited carrageenan-induced paw edema in rats, like BW755C (also known to be a synthetic LOX (lipoxygenase) and COX (cyclooxygenase)) inhibitors. Methanolic extract (M.E.) reduced migration of leukocyte and exudation of protein in peritoneal fluid, thus signifying its effectiveness in suppressing peritoneal inflammation. Additionally, M.E. also significantly inhibited the activity of COX (1 and 2) and 5-LOX. In LPS-activated peripheral blood mononuclear cells (PBMCs; TRAP), preincubation of the methanolic extract suppressed the formation of proinflamma- toiy cytokines (TNF-a and IL-6) [43].

Lupeol (0-80 pM) exerted anti-inflammation activity in RAW 264.7 cells and BMDMs (bone marrow-derived macrophages) stimulated by LPS. In a dose-dependent manner, it might suppress the activation, formation, and migration of osteoclastogenesis of macrophages. In arthritic mice, lupeol ameliorated inhibition of propagation of inflammation-related cytokines, clinical symptoms, and bone erosion. A significant reduction was observed in the accumulation of (18)-F-fluorodeoxyglucose ((18)-F-FDG) in the joints of arthritic mice [44].

IBD (Inflammatory bowel disease) i.e., Crohn’s disease and ulcerative colitis are chronic inflammatory diseases of lower GIT (gastrointestinal tract). Lupeol significantly decreased the formation of pro-inflammatory cytokines (IL-1 /?, TNFa, IL-6, and IL-12), and caused remarkable elevation in formation of p38 МАРК [39]. In vivo, in silico, ex vivo and in vitro studies revealed that Lupeol significantly prevented hemorrhage, oxidative stress, cleavage of collagen and CX3CR1 receptors, edema, myotoxicity, dermo- nectosis, and myonecrosis in inflammatory cell induced due to Echiscari- natus (saw-scaled viper) bite venom [34]. Intraperitoneal injection of Lupeol (@ 10,25, or 50 nig/kg) had significant effect on the severity of pancreatitis, which was proven by decreased neutrophil infiltration and pancreatic edema.

Additionally, lupeol suppressed the elevated content of digestive enzymes (IL-6) and cerulean-induced acinar cell death [54].


Extracts from turmeric (@ 1 or 10 pg/mL for 14 hours) reduced LPS (50 to lOOngmL-1), stimulated 1Ь-1Д and TNF-a formation of THP-1 cells analyzed by ELISA. LPS-stimulated IRAkl, 1кВа degradation, TLR4-MyD88 interaction, TLR4 expression, and МАРК activation were noteworthy decreased by turmeric. It also attenuated the IL-1/?, aortic iNOS expression, TNF-a, vascular dysfunction, and nitrite. It also induced apoptosis and increased PARP-1 and caspase-3 activation in HL-60 cells [58].

In ovariectomy (OVX) rats, curcumin, and tetrahydrocurcumin (THC) have revealed alike effectiveness for skin tail temperature, while THC prohibited glucose intolerance involved in aggravating osteoarthritis. Both these experimented components helped in protection from symptoms of osteoarthritis and behavior related to pain more compared to 17/?-estradiol treatment in estrogen-deficient rats. Along with this, they preserved lean body mass; and fat mass was reduced equal to that of 17/?-estradiol treatment. Symptoms of osteoarthritis were improved due to reduced expressions of ММРЗ, MMP13, TNF-a, IL-1/?, IL-6, and matrix metalloproteinases genes in the articular cartilage [59].

In the anti-inflammatory role, curcumin decreased the damage of skeletal muscle and fibrosis-related to ischemic injury. ELISA and immunohis- tochemical staining were performed to validate the mechanistic approach in curcumin-arbitrated protection of tissue. It led to reduced macrophage infiltration and decreased the responses of inflammation, as revealed by decreased IL-6, TNF-a, and IL-1 levels. Conclusively in macrophage, curcumin had inhibitory action on NF-кВ activation stimulated by LPS [45].

In intracerebral hemorrhage (ICH)-induced secondary brain injury, curcumin elevated neurological scores and decreased brain edema. In the mouse brain, it also minimized the expression of IL-17, VCAM-1 (vascular cell adhesion molecule-1), and INF-y, post 72 hours induction of ICH. The results proposed that administration of curcumin might have alleviated cerebral inflammation due to ICH, causing reduction in infiltration of T-lymphocytes into the brain [47].

Curcumin (@200 mg kg-1) minimized the expression of inflammatory cytokine, reduced lipid peroxidation and oxidative stress, prohibited apoptotic conditions, and elevated activity of antioxidative defense mechanism compared to saline or MP (methylprednisolone) treatment. Ultra structural and histopathological abnormalities were decreased in curcumin-administrated rats compared with saline-subjected and MP-subjected groups [32, 48].


In LPS-stimulated HT-29 cells, morin, vanillic acid, p-coumaric acid, and epicatechin from onion peels downregulated TNF-a mRNA expression, up-regulated the expression of HO-1 and GSTs (glutathione S-transferase) detoxification genes like GSTP1, GSTT1, and GSTM1 [44]. Quercetin lowered the mesenteric fat weights, increased the adiponectin mRNA levels, and lowered the IL-6 mRNA levels.

By influencing the adipokine expression, quercetin addressed obesity- induced inflammation [4]. Quercetin decreased level of tissue NO and TNF-a. Further, in vivo studies have provided the evidence for protective effect of Welsh onion green leaves (WOE’s) due to the decrease in lipid-oxidation and elevation in concentration of AOE (i.e., CAT (catalase), SOD (superoxide dismutase), and GPx (glutathione peroxidase)). In mice models, it also reduced formalin-induced pains and number of acetic acid-induced writhing responses [11]. Quercetin affected expression of gene and formation of Th-1- derived IFN-y, along with down-regulating the production of Th-2-derived IL-4 by means of normal peripheral blood mononuclear cells [57]. It is due to the anti-inflammatory potential of quercetin that prevents from formation of secondary infection trailed by disturbance in skin barriers [33].

The anti-inflammatory potential of quercetin is related to inhibitory action of lipoxygenase and retardation of inflammation-causing mediators. Quercetin boosts immunity and reduces inflammation by targeting various intracellular targeting phosphatases and kinases, membrane proteins and leukocytes. It suppresses the formation and migration of histamine and other inflammatory substances due to stabilization of cell membranes in mast cells [31]. Quercetin also inhibits activation of human mast cells via inhibiting the release of histamine, prostaglandins, leukotrienes, and Ca2+ influx. Mast-cells are dominant immunity-enhancing cells significant in autoimmune diseases and pathogenesis of allergic responses. Release of various cytokines like TNF and IL-8 responsible for inflammatory reactions in body are affected by the administration of quercetin. Therefore, quercetin is significant in the treatment of allergic inflammatory diseases (RA, asthma, and sinusitis) [17].

In clinical trials, quercetin @ 0.01 pM was incubated for fifteen minutes with human umbilical cord blood-derived cultured mast-cells grown in the presence of IL-6 and stem cell factor. The results indicated that inhibition (82%) of TNF-a, IL-6, and IL-8 occurred due to application of quercetin; however, histamine, and tryptase were reduced by 52-77% and 79-96%, respectively. Likewise, in human mast cells, the impact of quercetin on pro-inflammatory cytokines expression was also examined. Outcomes of this investigation revealed that quercetin reduced the expression of gene and formation of IL-1/?, IL-8, IL-6, and TNF-a in experimented human mast-cells. Administration of quercetin reduced phorbol calcium ionophore- induced activation of p38 МАРК and NF-kB [40].

Research studies on the inhibiting potential of black seed, chamomile, caraway, anise, cardamom, and fennel on histamine content revealed that combination of various herbs controlled the release of histamine from immunological (85%) and chemical (81%) induction of cells. Comparatively, quercetin was more effective in preventing histamine release by 95% and 97%, respectively [39].

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