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Immunohistochemical evaluation of interleukin-23 and cyclooxygenase-2 in the muscles of mice infected with Trichinella spiralis

El-Aswad BEW, Ammar AI, Mahmoud SF, Soliman SS, Abd El-Atty AF

Trop Biomed, 2020 Mar 01;37(1):75-88.
PMID: 33612720

The course of Trichinella (T.) spiralis infection includes intestinal and muscle phases. The aims of this work were to evaluate IL-23 and cyclooxygenase-2 (COX-2) by immunohistochemistry in the muscles of T. spiralis infected mice in a time-course study and to correlate their level with the serum levels of IL-23, IFN-γ, IL-4 and IL-10 cytokines. The mice were divided into an un-infected control group (UC) (10 mice) and 5 infected mouse groups (each 10 mice/group. Each mouse was infected with 200 T. spiralis larvae) and sacrificed on days 7, 14, 21, 28 and 35 post-infection (dpi). IL-23 showed weak expression (+1) on the 21st dpi, then it became moderately expressed (+2) on the 28th dpi and on day 35 pi, the immunoreactivity was strong (+3). COX-2 expressed weakly on 14 dpi, while the other mouse groups (21, 28 and 35) showed strong (+3) expression. IL-23 serum concentrations increased gradually in a significant pattern, in comparison to that of UC mice, from the 21st dpi to the end of the experiment. IFN-γ increased gradually and was significantly higher than those of UC mice from the 7th dpi, reached its maximum level on the 21st dpi, after which it decreased non-significantly. IL-4 up-regulated significantly in all infected groups in comparison to UC mice achieving its highest level on the 21st dpi and decreased after that. IL-10 increased significantly on the 7th dpi, but dropped at the 14th dpi, then reached its peak on the 21st dpi, and decreased again on the 28th and 35th dpi. In conclusion, T. spiralis infection caused increased expression of IL-23 and COX-2 in the muscle of infected mice, the effect being strongest on the 35th day. Also, the infection induced a mixed Th1/Th2 profile with a predominance of Th2 at the early muscle phase, after which the immune repose became mainly Th2.

Matched MeSH terms: Cyclooxygenase 2/immunology*
Tocotrienols suppress proinflammatory markers and cyclooxygenase-2 expression in RAW264.7 macrophages

Yam ML, Abdul Hafid SR, Cheng HM, Nesaretnam K

Lipids, 2009 Sep;44(9):787-97.
PMID: 19655189 DOI: 10.1007/s11745-009-3326-2

Tocotrienols are powerful chain breaking antioxidant. Moreover, they are now known to exhibit various non-antioxidant properties such as anti-cancer, neuroprotective and hypocholesterolemic functions. This study was undertaken to investigate the anti-inflammatory effects of tocotrienol-rich fraction (TRF) and individual tocotrienol isoforms namely delta-, gamma-, and alpha-tocotrienol on lipopolysaccharide-stimulated RAW264.7 macrophages. The widely studied vitamin E form, alpha-tocopherol, was used as comparison. Stimulation of RAW264.7 with lipopolysaccharide induced the release of various inflammatory markers. 10 mcirog/ml of TRF and all tocotrienol isoforms significantly inhibited the production of interleukin-6 and nitric oxide. However, only alpha-tocotrienol demonstrated a significant effect in lowering tumor necrosis factor-alpha production. Besides, TRF and all tocotrienol isoforms except gamma-tocotrienol reduced prostaglandin E(2) release. It was accompanied by the down-regulation of cyclooxygenase-2 gene expression by all vitamin E forms except alpha-tocopherol. Collectively, the data suggested that tocotrienols are better anti-inflammatory agents than alpha-tocopherol and the most effective form is delta-tocotrienol.

Matched MeSH terms: Cyclooxygenase 2/immunology
Cardamonin from Alpinia rafflesiana inhibits inflammatory responses in IFN-γ/LPS-stimulated BV2 microglia via NF-κB signalling pathway

Chow YL, Lee KH, Vidyadaran S, Lajis NH, Akhtar MN, Israf DA, et al.

Int Immunopharmacol, 2012 Apr;12(4):657-65.
PMID: 22306767 DOI: 10.1016/j.intimp.2012.01.009

The increasing prevalence of neurodegenerative diseases has prompted investigation into innovative therapeutics over the last two decades. Non-steroidal anti-inflammatory drugs (NSAIDs) are among the therapeutic choices to control and suppress the symptoms of neurodegenerative diseases. However, NSAIDs-associated gastropathy has hampered their long term usage despite their clinical advancement. On the natural end of the treatment spectrum, our group has shown that cardamonin (2',4'-dihydroxy-6'-methoxychalcone) isolated from Alpinia rafflesiana exerts potential anti-inflammatory activity in activated macrophages. Therefore, we further explored the anti-inflammatory property of cardamonin as well as its underlying mechanism of action in IFN-γ/LPS-stimulated microglial cells. In this investigation, cardamonin shows promising anti-inflammatory activity in microglial cell line BV2 by inhibiting the secretion of pro-inflammatory mediators including nitric oxide (NO), prostaglandin E(2) (PGE(2)), tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6). The inhibition of NO and PGE(2) by cardamonin are resulted from the reduced expression of inducible nitric oxide synthase (iNOS) and cycloxygenase-2 (COX-2), respectively. Meanwhile the suppressive effects of cardamonin on TNF-α, IL-1β and IL-6 were demonstrated at both protein and mRNA levels, thus indicating the interference of upstream signal transduction pathway. Our results also validate that cardamonin interrupts nuclear factor-kappa B (NF-κB) signalling pathway via attenuation of NF-κB DNA binding activity. Interestingly, cardamonin also showed a consistent suppressive effect on the cell surface expression of CD14. Taken together, our experimental data provide mechanistic insights for the anti-inflammatory actions of cardamonin in BV2 and thus suggest a possible therapeutic application of cardamonin for targeting neuroinflammatory disorders.

Matched MeSH terms: Cyclooxygenase 2/immunology
Anti-neuroinflammatory responses in lipopolysaccharide-stimulated BV2 microglial cells upon treatment with methanol extract of Panax ginseng root

Chien Yi K, Anna Pick Kiong L, Ying Pei W, Rhun Yian K, Sobri H

J Tradit Chin Med, 2021 04;41(2):185-193.
PMID: 33825397

OBJECTIVE: To investigate the anti-neuroinflammatory properties of Panax ginseng (P. ginseng) root by measuring the levels of nitric oxide (NO), tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) in lipopolysaccharide (LPS)-stimulated BV2 microglia cells.
METHODS: Maximal non-toxic dose (MNTD) of methanol extract of P. ginseng root culture on BV2 microglia cells was first determined via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, followed by treatment and LPS stimulation of cells, and the measurement of NO using Griess assay and TNF-α, IL-6, and IL-10 using ELISA assay.
RESULTS: The MNTD of P. ginseng root extract was determined to be (587 ± 57) µg/mL. Following that, NO and IL-6 levels were found to be insignificantly reduced by 6.88% and 0.14% respectively in stimulated cells upon treatment with MNTD. Treatment with MNTD yielded similar insignificant result, with only a reduction of 3.58% and 0.08% in NO and IL-6 levels respectively. However, TNF-α and IL-10 levels were significantly downregulated by 15.64% and 34.96% respectively upon treatment with P. ginseng root extract at MNTD.
CONCLUSION: Methanol extract of P. ginseng root culture did not show any significant anti-inflammatory effects on NO and IL-6 levels, but might potentially possess both anti-neuroinflammatory and pro-neuroinflammatory properties through the downregulation of TNF-α and IL-10 respectively.

Matched MeSH terms: Cyclooxygenase 2/immunology