Potential effects of samsum ant, Brachyponera sennaarensis, venom on TNF-α/NF-κB mediated inflammation in CCL4-toxicity in vivo

Abstract

BackgroundAnt venom shows antimicrobial, anti-parasitic and anti-inflammatory activities, both in vitro and in vivo. Our recent studies have confirmed the role of samsum ant venom (SAV) as a powerful antioxidant. This study aimed to investigate whether SAV as a potential treatment for CCl4-induced acute liver toxicity in an animal (rat) model.MethodsThirty-two rats were assigned into four groups; the first one served as the control. The second group received a single dose of 1 ml/kg CCl4 in a 1:1 ratio with olive oil through an intraperitoneal injection. The third group received a single dose of 1 ml/kg CCl4 and then treated with SAV at a dose of 100 μg SAV twice a week for three weeks. The fourth group received a dose of 100 μg SAV only twice a week for three weeks. ELISA, RT-PCR and histopathological examinations were applied.ResultsResults showed that antioxidant enzymes were significantly reduced in the diseased animals. SAV was found to significantly restore the oxidative stability in diseased animals. ELISA estimation and RT-PCR analysis also showed significant upregulation of both nuclear factor (κB) NF-κB and inhibitor (κB) IκB, respectively, in the diseased animals compared to the normal ones. The expression of tumour necrosis factor alpha (TNF-α) and pro-apoptotic receptor (Fas) were also significantly up-regulated in the diseased rats. Interestingly, SAV was found to significantly restore NF-κB, IκB and TNF-α in the diseased rats to the normal values. As a result, liver enzymes, serum proteins and lipid concentrations were significantly improved by SAV in CCl4-animals in comparison with the control ones. Moreover, SAV obviously improved the hepatic tissues of the same group was.ConclusionSAV treatment restores the normal biochemical and oxidative stability by improving the TNF-α/NF-κB mediated inflammation in CCL4-treated rats.

The Liver Protection Effects of Maltol, a Flavoring Agent, on Carbon Tetrachloride-Induced Acute Liver Injury in Mice via Inhibiting Apoptosis and Inflammatory Response

“…TNF-α can induce pleiotropic cytokines produced by a variety of physiological and pathological conditions [ 39 ]. This is related to the products of inflammation and fibrosis, and regulates cytokines to a certain extent, but this is not the direct cause of hepatic cell necrosis induced by CCl 4 [ 40 , 41 ]. Inflammation might directly activate the intracellular death signals and lead to deleterious outcomes [ 42 ].…”

Anti-inflammatory activities of arthropod peptides: a systematic review

“… Animal (Source) Peptide Access number Activity as inflammatory mediator Ref. Insect Pseudomyrmex triplarinus Pseudomyrmecitoxin-Pt1 subunit LS1 P0DSL7 Antidematogenic effect [ 19 - 21 ] Pseudomyrmecitoxin-Pt1 subunit SS3 P0DSM1 Pseudomyrmecitoxin-Pt1 subunit LS2 P0DSL8 Pseudomyrmecitoxin-Pt1 subunit SS2 P0SDM0 U1-pseudomyrmecitoxin-Pt1 subunit SS1 P0DSL9 Paraponera clavata Delta-paraponeritoxin-Pc1a P41736 Edema reduction, antinociceptive [ 22 ] Dinoponera quadríceps Venom peptides (Extract) C0HJK0 Suppression of inflammatory mediators [ 23 - 26 ] Brachyponera sennaarensisare Venom peptides (Extract) - Regulate the expression of MHC-II, CD80 y CD-86, IFN-γ and IL-17 [ 28 , 29 ] Pachycondyla sennaarensis Venom peptides (Extract) - Regulate NF-kB, kinase IkB, TNF-α and Fas ...…”

“…The B. sennaarensisare toxins regulate the expression of MHC-II, CD80, and CD-86, as well as interferon- γ (IFN-γ) and interleukin-17 (IL-17), mediators that are involved in various chronic pathologies and cancer as demonstrated after in vivo tests [ 28 ]. Furthermore, these peptides can regulate the nuclear factor kappa B (NF-kB), kinase IkB upward, and suppress nuclear transcription factor-α (TNF-α) and the cell surface death receptor (Fas), although the mechanism involved in anti-inflammatory activity has not been fully elucidated [ 29 , 30 ].…”

Neoagarooligosaccharide Protects against Hepatic Fibrosis via Inhibition of TGF-β/Smad Signaling Pathway

“…CCl 4 , a well-known fibrosis-inducing hepatotoxin, is extensively used in liver-related studies. CCl 4 -treated rodents exhibited fatty changes along with an increase in inflammatory cell infiltrations, damage to normal hepatocytes, deposition of collagen and formation of fiber segmentation [ 26 ]. Chronic liver toxicity induced by CCl 4 causes an increase in lipid peroxidation that leads to a decrease in antioxidant enzymes and glutathione activities [ 27 , 28 ].…”