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Limited GADD45α expression and function in IL-1β toxicity towards insulin-producing cells

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Skalniak L., Gurgul-Convey E., Okreglicka K., Skalniak A., Jura J.
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2013
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vol. 60
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issue 4
595-602
EN
Growth arrest and DNA damage-inducible (GADD) 45 proteins are regulators of cell death and survival. The proinflammatory cytokine IL-1β strongly increases the level of the transcript encoding GADD45α in rat insulin-producing INS-1E cells. The activation of Gadd45α gene is clearly dependent on JNK and NF-κB activation and the synthesis of the secondary mediator nitric oxide (NO). Interestingly, the observed twelve-fold increase in the GADD45α-coding transcript level is not followed by increased expression of GADD45α at the protein level. An analysis of IL-1β toxicity in INS-1E cells overexpressing GADD45α revealed no correlation between the GADD45α protein level and the sensitivity to IL-1β toxicity. These findings suggest that the potential engagement of GADD45α in IL-1β toxicity towards beta cells is limited to the effects induced by the basal expression level of this protein.
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Mutual relations between the amygdala and pro-inflammatory cytokines: IL-1β and IL-6

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Czerwiec K., Ruciński J., Piwko G., Myślińska D., Kosiński A.
European Journal of Translational and Clinical Medicine
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2022
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vol. 5
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issue 1
40-46
EN
Interleukin 1 (IL-1) and interleukin 6 (IL-6) are typical examples of multfunctonal pro-infammatory cytokines involved in the regulaton of the immune response, hematopoiesis, and infammaton. Both peripheral and intraventricular administraton of these cytokines causes acute phase symptoms, e.g. fever, actvaton of the hypothalamic-pituitary-adrenal axis and psychological depression. The amygdala belongs to the structures of the limbic system involved in the regulaton of the immune response. Increased actvity of immune system may lead to changes in the role of amygdala, medial prefrontal cortex, anterior cingulate cortex or insula. The aim of the study was to present the mutual interactons between the amygdala and pro-infammatory cytokines such as interleukin-1β (IL-1 beta) and interleukin 6 (IL-6). Most of the data included in this review comes from animal studies.
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Effects of hypothermia on skeletal ischemia reperfusion injury in rats

63%
Ekinci Ş., Kaldırım Ü., Akyıldız F., Bilgiç S., Koca K., Poyrazoğlu Y., Uysal O. S., Turğut H., Türkkan S., Erşen Ö., Topal T., Ozkan H.
Open Medicine
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2014
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vol. 10
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issue 1
EN
Objective: The aim of this study was to investigate the effect of hypothermia (H) on skeletal ischemia-reperfusion (IR) injury in rats by measuring malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), nitric oxide (NO), and interleukin-1 beta (IL-1β) in muscle, and measureing immunohistochemical- inducible nitric oxide synthase (iNOS) staining of skeletal muscle. Materials and Methods: Eighteen Wistar Albino rats were divided randomly into three groups (sham, IR, hypothermia) (n=6). The sham group had all procedures without the IR period. The lower right extremity of rats in the IR and hypothermia groups was subjected to 2 hours of ischemia and 22 hours of reperfusion by applying a clamp on the common iliac artery and a rubber-band at the level of the lesser trochanter under general anesthesia. Rats in the hypothermia group underwent 4 hours of hypothermia during the first four hours of reperfusion in addition to a 2-hour ischemia and 22-hour reperfusion period. All rats were sacrificed at end of the IR period using a high dose of anesthesia. The tibialis anterior muscles were preserved. Immunohistochemical iNOS staining was performed, and MDA, SOD, GSH-Px, NO, and IL-1β were measured in the muscle. Results: The level of MDA, NO, and IL-1β in muscle was increased in the IR group compared with that in the sham group, but these parameters were decreased in the hypothermia group compared with the IR group. The activities of SOD and GSH-Px in muscle were decreased in the IR group; however, these parameters were increased in the hypothermia group. The score and intensity of iNOS staining of skeletal muscle was dens in IR group, mild in hypothermia group, and weak in sham group. Conclusion: The present study has shown that hypothermia reduced IR injury in the skeletal muscle by decreasing the levels of MDA, NO, and IL-1β, and increasing the activities of SOD and GSH-Px. In addition, hypothermia attenuated the score and intensity of iNOS staining.
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