Time course of carrageenin inflammation under treatment with lithium hydroxybutyrate

Aleksandrov, P. N.; Speranskaya, T. V.

doi:10.1007/bf00840397

Cited by 2 publications

(3 citation statements)

References 4 publications

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“…(C) Semiquantitative densitometric analysis of immunoblots revealed that expression of p-GSK3b inversely correlates with expression of CD45 (p < 0.05; n = 20). lithium, a first-generation GSK3b inhibitor, suppressed inflammatory responses induced by zymosan (62) or carrageenin (63) and ameliorated inflammation in vivo in rats with the Arthus reaction (64) or allergic encephalomyelitis (65). Overall, evidence establishes GSK3b inhibition as a novel therapy for inflammatory human disease, including proliferative kidney disease (66).…”

Section: Discussionmentioning

confidence: 96%

Glycogen Synthase Kinase 3β: A Novel Marker and Modulator of Inflammatory Injury in Chronic Renal Allograft Disease

Gong

Chen

et al. 2008

American Journal of Transplantation

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One key cell-signaling event central to inflammation in kidney diseases, including chronic renal allograft dysfunction or disease (CRAD), is the activation of NF-j B, which controls transcription of numerous proinflammatory mediators. Glycogen synthase kinase (GSK) 3b is an indispensable element of NF-j B activation, however, the exact role of GSK3b in the pathogenesis of inflammatory kidney diseases like CRAD is uncertain and was examined. Immunohistochemistry staining of GSK3b was weak in normal kidneys, but was markedly induced in inflamed allograft kidneys, with prominent cytoplasmic staining of tubular cells in areas of inflammation. Net GSK3b activity is regulated by inhibitory phosphorylation of its serine 9 residue, and this occurred in CRAD. Thus, the magnitude of GSK3b inactivation was inversely correlated with the degree of injury as assessed by Banff criteria. In vitro in cultured human tubular epithelial cells, GSK3b overexpression augmented, while GSK3b silencing diminished proinflammatory cellular responses to TNF-a stimulation, including NF-j B activation and expression of chemokines MCP-1 and RANTES. These inflammatory responses were obliterated by GSK3b inhibitors. Collectively, GSK3b plays an important role in mediating proinflammatory NF-j B activation and renal inflammation. Suppression of GSK3b activity might represent a novel therapeutic strategy to treat CRAD.

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Section: Discussionmentioning

confidence: 96%

Glycogen Synthase Kinase 3β: A Novel Marker and Modulator of Inflammatory Injury in Chronic Renal Allograft Disease

Gong

Chen

et al. 2008

American Journal of Transplantation

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“…These experiments described inflammation induced by carrageenan after application to the cheek of guinea-pigs (Yavuz and Akbay 1989) and to the cheek pouch in hamsters (Aleksandrov et al 1986;Aleksandrov and Speranskaya 1988). However, it is difficult to make valid comparisons between our work and these earlier studies, for a variety of reasons.…”

Section: Discussionmentioning

confidence: 62%

“…For instance, only the abstracts are in English and these do not mention the doses of carrageenan used or the time course of the inflammation. Moreover, the inflammatory variables measured were different-''pathological process' ' Aleksandrov et al 1986; changes in the microvasculature (Aleksandrov and Speranskaya 1988) and histopathological changes (Yavuz and Akbay 1989). Finally, comparison of inflammation between species adds a new layer of assumptions that weaken the strength of that assessment.…”

Section: Discussionmentioning

confidence: 99%

Tissue-selective inflammation in the oral cavity of the rat

et al. 2016

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In the current study, carrageenan (CG; 100-1000 μg/site) was injected intraorally in the cheeks of Holtzman or Wistar rats to evaluate the consequences of administration of a non-immunogenic stimulus in the orofacial region. Subsequent inflammation was measured as oedema (increased thickness of the cheek wall using digital calipers), relative to the other cheek injected with saline. Oedema formation and tissue collection for histopathological studies were assessed at 0.5, 1, 2, 3, 4, 6, 24, 48, 72, 96, 120 and 144 h after injection. In parallel, other groups of rats were injected with CG in the hind paw, to provide a reference response. The inhibitor of prostaglandin biosynthesis, indomethacin, and antagonists of histamine, serotonin and NK1 receptors were injected s.c., 0.5 h before CG. CG induced a dose-related oedema more rapidly from 0 to 2 h which lasted for at least 72 h, showing a biphasic profile (peak at 2 and 24 h), compared with the monophasic oedema induced in rat paws (maximal duration of 24 h). Histopathological analysis of the CG-injected cheek revealed oedema formation with little leukocyte recruitment at 1-3 h, mast cell degranulation at 6 h, and a mixed polymorphonuclear and mononuclear cell infiltrate by 24 h. Histamine and serotonin antagonists and indomethacin, but not the NK1 antagonist, decreased cheek oedema in the first 4 h following carrageenan. Taken together, our data indicated important differences in the pattern of inflammation between the oral cavity and the paw which will determine the therapeutic approach to the treatment of inflammatory conditions in the oral cavity.

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Time course of carrageenin inflammation under treatment with lithium hydroxybutyrate

Cited by 2 publications

References 4 publications

Glycogen Synthase Kinase 3β: A Novel Marker and Modulator of Inflammatory Injury in Chronic Renal Allograft Disease

Glycogen Synthase Kinase 3β: A Novel Marker and Modulator of Inflammatory Injury in Chronic Renal Allograft Disease

Tissue-selective inflammation in the oral cavity of the rat

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