Inhibitory effect of a new orally active cedrol-loaded nanostructured lipid carrier on compound 48/80-induced mast cell degranulation and anaphylactic shock in mice

Chakraborty, Shreyasi; Kar, Nabanita; Kumari, Leena; De, Asit K.; Bera, Tanmoy

doi:10.2147/ijn.s132114

Cited by 31 publications

(19 citation statements)

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“…As observed in this work, other authors also demonstrated the efficiency of C48/80 in inducing anaphylactoid shock in mice (14,27,28), rats (15,29), guinea pigs (30), rabbits (18), and pigs (9). The ability of C48/80 to promote a direct release of nitric oxide from endothelial cells was confirmed by a significant increase in nitric oxide plasma levels.…”

Section: Discussionsupporting

confidence: 81%

Effects of NO/cGMP inhibitors in a rat model of anaphylactoid shock

Albuquerque

Ferreira

Carvalho

et al. 2020

Braz J Med Biol Res

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Anaphylactic shock can be defined as an acute syndrome, and it is the most severe clinical manifestation of allergic diseases. Anaphylactoid reactions are similar to anaphylactic events but differ in the pathophysiological mechanism. Nitric oxide (NO) inhibitors during anaphylaxis suggest that NO might decrease the signs and symptoms of anaphylaxis but exacerbate associated vasodilation. Therefore, blocking the effects of NO on vascular smooth muscle by inhibiting the guanylate cyclase (GC) would be a reasonable strategy. This study aimed to investigate the effects of NO/cGMP pathway inhibitors methylene blue (MB), N o-nitro-L-arginine methyl ester hydrochloride (L-NAME), and indigo carmine (IC) in shock induced by compound 48/80 (C48/80) in rats. The effect was assessed by invasive blood pressure measurement. Shock was initiated by C48/80 intravenous bolus injection 5 min before (prophylactic) or after (treatment) the administration of the inhibitors MB (3 mg/kg), L-NAME (1 mg/kg), and IC (3 mg/kg). Of the groups that received drugs as prophylaxis for shock, only the IC group did not present the final systolic blood pressure (SBP) better than the C48/80 group. Regarding shock treatment with the drugs tested, all groups had the final SBP similar to the C48/80group. Altogether, our results suggested that inhibition of GC and NO synthase in NO production pathway was not sufficient to revert hypotension or significantly improve survival.

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Section: Discussionsupporting

confidence: 81%

Effects of NO/cGMP inhibitors in a rat model of anaphylactoid shock

Albuquerque

Ferreira

Carvalho

et al. 2020

Braz J Med Biol Res

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“…37 However, more recent work by Chakraborty et al in murine mast cell culture clearly shows a robust concentration-dependent effect of cromolyn in blocking 48/80 evoked calcium influx and degranulation (as measured by release of histamine and ß-hexaminidase) and prevented 48/80-induced shock. 38 Furthermore, though indirect, it has been reported that the effects of intracerebral 48/80 in mice (leading to brain mast cell degranulation) on behavior were blocked by intracranial delivery of cromolyn, suggesting an action on murine brain mast cells. 39 With regard to the hypothesized role of mast cells, two additional issues must be considered.…”

Section: Role Of Mast Cells In Compound 48/80 Actionsmentioning

confidence: 99%

Role of Toll-like receptor 4 signaling in mast cell-mediated migraine pain pathway

et al. 2019

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Degranulation of meningeal mast cells leading to the sensitization of trigeminal vascular afferent processing is believed to be one of the mechanisms underlying the migraine pain pathway. Recent work suggests that Toll-like receptor 4 (TLR4) may be involved in signaling states of central sensitization. Using a murine model of light aversion produced by compound 48/80 (2 mg/kg, intraperitoneal) mast cell degranulation, employed as a surrogate marker for photophobia observed in migraineurs, we examined the role of TLR4 in migraine-like behavior and neuronal activation. Using a two-chambered light/dark box, we found that compound 48/80 administration in male and female C57Bl/6 mice produced light aversion lasting up to 2 h, and that pre-treatment with sumatriptan (1 mg/kg, i.p.) reliably prevented this effect. Genetic deletion and pharmacological blockade of TLR4 with TAK-242 (3 mg/kg, i.p.) reversed the light aversive effects of compound 48/80 in males but not in females. Assessing the downstream signaling pathway in mutant mice, we found that the TLR4-mediated, light aversion was dependent upon myeloid differentiation primary response gene 88 but not Toll-interleukin-1 receptor domain-containing adapter-inducing interferon-β signaling. In separate groups, male mice sacrificed at 10 min following compound 48/80 revealed a significant increase in the incidence of evoked p-extracellular signal–regulated kinases (+) neurons in the nucleus caudalis of wild type but not Tlr4 −/− mice or in mice pre-treated with sumatriptan. This study thus provides the first evidence for involvement of TLR4 signaling through MyD88 in initiating and maintaining migraine-like behavior and nucleus caudalis neuronal activation in the mouse.

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“…The zeta potential value provides us with evidence regarding the surface charge of the NPs, and this appeared to be more negative than previously reported. [42][43][44] Additionally, it gives us an idea about the stability of the NPs and the zeta potential value obtained for the Zn-doped C. roseus NPs lies within the low stable range, implying that the green NPs are unstable in aqueous solution. Therefore, there may be possible aggregations due to residual surfactants.…”

Section: Resultsmentioning

confidence: 99%