Sentence examples for mouse ear oedema from inspiring English sources

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Awad isolated the steroid 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien 3-O-β-d-glucopyranosyl-stigmasta-5,25-dien

The tested extracts were able to decrease the mouse ear oedema induced by xylene.

Eupatorin has been shown to have anti-inflammatory effects in a mouse ear oedema model [ 7] as well as antiproliferative activity in human gastric adenocarcinoma (MK-1), human uterus carcinoma (HeLa), and murine melanoma (B16F10) cell lines [ 6].

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Additionally, compound 7a blocked mice ear inflammation by 67% and suppressed the accumulation of inflammatory cells in an in vivo mouse ear edema evaluation.

Xylene-induced mouse ear edema model: Male ICR mice weighting 18 20 g were used.

The results of mice ear edema depicted significant inhibition of ear edema (76.37 ± 12.52%; p < 0.05).

The results showed that EE (200 mg/kg) exhibited significant (p < 0.05) suppression of arachidonic acid and xylene-induced ear oedema in mice, while the effect of IC (400 and 600 μg/kg) is more pronounced (p < 0.01) (Fig.  4b).

Xylene-induced ear oedema in mice was selected to evaluate acute anti-inflammatory activity and is a good in vivo test useful for evaluating lipoxygenase inhibitors and partially associated with substance P [ 44].

In the arachidonic acid induced ear oedema model in mice, single or multiple administration of an emulsion containing 1.5% was capable of significantly reducing the inflammatory oedema.

Phomol, 4-arylcoumarins and ergoflavin produced by endophytes showed anti-inflammatory activity using reporter gene assays and in ear oedema model in mice [ 17], murine macrophage RAW 264.7 cells [ 18] and human monocytic cell line [ 19], respectively.

In the mouse ear, berteroin suppressed TPA-induced edema formation by down-regulating COX-2, NF-κB and ERK [33].

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