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Abstract: Aim: This study evaluated the anti‐inflammatory properties of a species of Sorghum bicolor leaf (SBL) grown in West Africa. Method: Cyclo‐oxygenase (COX)‐2:COX‐1 selectivity assay was carried out by plating isolated peripheral blood mononuclear cells in culture medium with specific SBL fractions: crude extract (J), ethyl‐acetate (JE) and aqueous (JA); secondary compounds from JE (JE5, JE6, JE7 and JE8); purified (P9) and semi‐purified (P8) compounds from JE5 at 5‐200 μg/mL for 1 hour. Test compounds and controls ibuprofen (50 μmol/L) and CAY10404 (1 μmol/L; 10 μmol/L) were added to two sets of plates, one without lipopolyshaccharide (LPS) and the other with LPS (1 μg/mL) for 24 hour. COX‐2IC50:COX‐1IC50 ratio represented 50% inhibition of the activity of COX‐2 to that of COX‐1 using ibuprofen as control. In separate experiments the supernatant of P8 and P9‐treated fractions of SBL and controls were plated with RAW 264.7 macrophage cells to measure prostaglandin (PG)‐E2 production and cell proliferation activity. Results: JA fraction of SBL had the highest ratio of COX‐2IC50:COX‐1IC5041.214 whereas JE had the lowest ratio COX‐2IC50:COX‐1IC501.161. Interestingly, JE5 derived from JE showed a ratio of COX‐2IC50:COX‐1IC500.495 while P8 derived from JE5 showed a dose‐dependent reduction in COX‐2IC50:COX‐1IC50 ratio and in PG‐E2 production, which was more effective compared to ibuprofen. A dose‐dependent reduction in RAW 264.7 macrophage cell proliferation was also observed in P8‐treated cells. The phenolic compounds identified in P8 include apigenin and apigeninidin adducts which may explain the exceptional anti‐inflammatory activity and efficacy in COX‐2 targeting. [ABSTRACT FROM AUTHOR]

Vitex spp. have been reported as constituents of herbal preparations, namely Vitex peduncularis , commonly used in Asian countries. Unlike other species extensively investigated, reports on the biological activities and chemical profile of V. peduncularis are still scarce. In this work, the polyphenolic profile of V. peduncularis stem bark was unveiled, revealing a high content of apigenin and luteolin derivatives. More than 20 polyphenols were identified and quantitated for the first time, including C -rhamnosyl flavones infrequently reported. Regarding potential anti-inflammatory properties, the methanolic extract of the stem bark significantly reduced the levels of NO in macrophages, which may be a consequence of scavenging effect upon • NO. Significant inhibition of phospholipase A 2 activity was also noted. Consequently, the therapeutic applicability of this edible plant is also broadened due to the anti-inflammatory properties found. [ABSTRACT FROM AUTHOR]

Apigenin is one of the plant flavonoids present in fruits and vegetables, acting as an important nutraceutical component. It is recognized as a potential antioxidant, antimicrobial, and anti-inflammatory molecule. In the present study, the mechanism of anti-inflammatory action of apigenin on lipopolysaccharide (LPS)-induced pro-inflammatory cytokines and activator protein-1 (AP-1) factors in human lung A549 cells was investigated. The anti-inflammatory activity of apigenin on LPS-induced inflammation was determined by analyzing the expression of pro-inflammatory cytokines, nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and different AP-1 factors. Apigenin significantly inhibited the LPS-induced expression of iNOS, COX-2, expression of pro-inflammatory cytokines (IL-1β, IL-2, IL-6, IL-8, and TNF-α), and AP-1 proteins (c-Jun, c-Fos, and JunB) including nitric oxide production. Study confirms the anti-inflammatory effect of apigenin by inhibiting the expression of inflammatory mediators and AP-1 factors involved in the inflammation and its importance in the treatment of lung inflammatory diseases. [ABSTRACT FROM AUTHOR]

This study aims to evaluate the possible mechanisms responsible for the anti-inflammatory effects of apigenin lipopolysaccharide (LPS)-induced inflammatory in acute lung injury. In this study, the anti-inflammatory effects of apigenin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and the possible mechanisms involved in this protection were investigated. Pretreatment with apigenin prior to the administration of intratracheal LPS significantly induced a decrease in lung wet weight/dry weight ratio in total leukocyte number and neutrophil percent in the bronchoalveolar lavage fluid (BALF) and in IL-6 and IL-1β, the tumor neurosis factor-α (TNF-α) in the BALF. These results showed that anti-inflammatory effects of apigenin against the LPS-induced ALI may be due to its ability of primary inhibition of cyclooxygenase-2 (COX-2) gene expression and nuclear factor kB (NF-kB) gene expression of lung. The results presented here suggest that the protective mechanism of apigenin may be attributed partly to decreased production of proinflammatory cytokines through the inhibition of COX-2 and NF-kB activation. The results support that use of apigenin is beneficial in the treatment of ALI. [ABSTRACT FROM AUTHOR]

Background: Apigenin is a non-toxic natural flavonoid that is abundantly present in common fruits and vegetables. It has been reported that apigenin has various beneficial health effects such as anti-inflammation and chemoprevention. Multiple studies have shown that inflammation is an important risk factor for atherosclerosis, diabetes, sepsis, various liver diseases, and other metabolic diseases. Although it has been long realized that apigenin has anti-inflammatory activities, the underlying functional mechanisms are still not fully understood. Methodology and Principal Findings: In the present study, we examined the effect of apigenin on LPS-induced inflammatory response and further elucidated the potential underlying mechanisms in human THP-1-induced macrophages and mouse J774A.1 macrophages. By using the PrimePCR array, we were able to identify the major target genes regulated by apigenin in LPS-mediated immune response. The results indicated that apigenin significantly inhibited LPS-induced production of pro-inflammatory cytokines, such as IL-6, IL-1β, and TNF-α through modulating multiple intracellular signaling pathways in macrophages. Apigenin inhibited LPS-induced IL-1β production by inhibiting caspase-1 activation through the disruption of the NLRP3 inflammasome assembly. Apigenin also prevented LPS-induced IL-6 and IL-1β production by reducing the mRNA stability via inhibiting ERK1/2 activation. In addition, apigenin significantly inhibited TNF-α and IL-1β-induced activation of NF-κB. Conclusion and Significance: Apigenin Inhibits LPS-induced Inflammatory Response through multiple mechanisms in macrophages. These results provided important scientific evidences for the potential application of apigenin as a therapeutic agent for inflammatory diseases. [ABSTRACT FROM AUTHOR]

Highlights: [•] Vitexin and isovitexin are C-glycosylated derivatives of apigenin. [•] Isovitexin was found as the most potent inhibitor against AR, AGE, and ChEs. [•] Vitexin showed the most potent PTP1B inhibitory activity. [•] Apigenin rather than vitexin and isovitexin showed anti-inflammatory activity. [•] C-glycosylation of apigenin might relate to intensity of respective bioactivities. [Copyright &y& Elsevier]

Abstract: Infection with Helicobacter pylori causes extensive gastric epithelial cell inflammation which may progress to atrophic gastritis, intestinal metaplasia, and even gastric adenocarcinoma. Apigenin (4′,5,7-Trihydroxyflavone) is widely distributed in fruits and vegetables, and is a well-known antiinflammatory supplement with low cytotoxicity. In this study, we investigated the anti-inflammatory effects of apigenin in H. pylori-infected MKN45 cells, for which IκBα, cyclooxygenase-2 (COX-2), intercellular adhesion molecule-1 (ICAM-1), reactive oxygen species (ROS), interleukin-8 (IL-8), IL-6, IL-1β, and mucin-2 (MUC-2) expressions were examined. Apigenin treatments (9.3–74μM) significantly increased the IκBα expression, and thus inhibited nuclear factor kappa B (NF-κB) activation, and the inflammatory factor (COX-2, ICAM-1, ROS, IL-6, and IL-8) expressions decreased. The ROS levels decreased partially based on the intrinsic scavenging property of apigenin. In summary, apigenin treatments effectively inhibited NF-κB activation and the related inflammatory factor expressions, as well as increased MUC-2 expression in the H. pylori-infected MKN45 cells. The compound shows great potential as a candidate agent for the inhibition of H. pylori-induced extensive gastric epithelial cell inflammation. [Copyright &y& Elsevier]

Abstract: Flavonoids are widely distributed in many fruits and plants, and it has been shown that most flavonoids have anti-inflammatory activity; however, the mechanisms of how the flavonoids exhibit their anti-inflammatory activity have not been clarified. We therefore focus on flavonoids Apigenin, Luteolin and Fisetin because of their related structure. We found that these compounds significantly inhibited TNFα-induced NF-κB transcriptional activation; however, they had no effect on the degradation of IκB proteins and the nuclear translocation and DNA binding activity of NF-κB p65. Interestingly, the suppression of NF-κB activation by these flavonoids is due to inhibition of the transcriptional activation of NF-κB, since the compounds markedly inhibited the transcriptional activity of GAL4-NF-κB p65 fusion protein. In addition, while Apigenin and Luteolin slightly inhibited TNFα-induced JNK activation, they had no effect on TNFα-induced activation of ERK and p38. Unexpectedly, Fisetin enhanced and sustained activation of ERK and JNK but not p38 in response to TNFα. Strikingly, TNFα-induced expression of CCL2/MCP-1 and CXCL1/KC was significantly inhibited by Apigenin and Luteolin but not Fisetin. Furthermore, the administration of Apigenin and Luteolin markedly inhibited acute carrageenan-induced paw edema in mice; however, Fisetin failed to have an effect. These observations strongly suggest that the slight structural difference in flavonoids may cause a defective effect of Fisetin on these inflammatory responses, and this may be due to the differences in their direction of the effect on the activation pathways of MAP kinases. [Copyright &y& Elsevier]