Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway

Zhao, Zijun; Li, Yishuai; Chi, Fei; Ma, Li; Li, Yanan; Hou, Zhiyong; Wang, Qiujun

doi:10.18632/aging.204461

Cited by 6 publications

(2 citation statements)

References 57 publications

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“…Another study revealed that sevoflurane alleviated hepatic IRI in mice by reducing oxidative stress and inflammatory response via the miR 218 5p/GAB2/PI3 K/AKT pathway. 37 Zhao et al 38 stated that postconditioning with sevoflurane reduced cerebral IR-induced neurological deficits in rats by suppressing neuroinflammatory responses through inhibition of the TLR4/MyD88/TRAF6 signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Effects of sevoflurane and fullerenol C60 on lower limb ischemia–reperfusion injury in streptozocin-induced diabetic mice

Polat,

Şengel,

Küçük

et al. 2024

Science Progress

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Background: Ischemia–reperfusion injury (IRI) poses a significant challenge for physicians, necessitating the management of cell damage and the preservation of organ functions. Various surgical procedures, such as vascular surgery on extremities, temporary cross-clamping of the abdominal aorta in aortic surgery, and the use of a tourniquet in extremity surgeries, may induce lower limb IRI. The susceptibility to IRI is heightened in individuals with diabetes. This study aimed to investigate the effects of fullerenol C60 and sevoflurane on mouse muscle tissue in a lower limb IRI model and to assess their potential in preventing complications arising from ischemia–reperfusion in mice with streptozocin-induced diabetes. Methods: A total of 36 adult Swiss albino mice were randomly divided into six groups, each consisting of six mice: control group (group C), diabetes group (group D), diabetes–ischemia/reperfusion group (group DIR), diabetes–ischemia/reperfusion–fullerenol C60 group (group DIR-FC60), diabetes–ischemia/reperfusion–sevoflurane group (group DIR-S), and diabetes–ischemia/reperfusion–sevoflurane–fullerenol C60 group (DIR-S-FC60). Streptozocin (55 mg/kg) was intraperitoneally administered to induce diabetes in the relevant groups, with mice displaying blood glucose levels of 250 mg/dL or higher at 72 h were considered diabetic. After 4 weeks, all groups underwent laparotomy under anesthesia. In DIR-FC60 and DIR-S-FC60 groups, fullerenol C60 (100 mg/kg) was intraperitoneally administrated 30 min before the ischemia period. Sevoflurane, delivered in 100% oxygen at a rate of 2.3% and 4 L/min, was administered during the ischemia period in DIR-S and DIR-S-FC60 groups. In the IR groups, a microvascular clamp was placed on the infrarenal abdominal aorta for 120 min during the ischemia period, followed by the removal of the clamp and a 120-min reperfusion period. At the end of the reperfusion, gastrocnemius muscle tissues were removed for histopathological and biochemical parameter examinations. Results: Histopathological examination revealed a significant reduction in the disorganization and degeneration of muscle cells in the DIR-S-FC60 group compared to the DIR group (p = 0.041). Inflammatory cell infiltration was notably lower in the DIR-S, DIR-FC60, and DIR-S-FC60 groups than in the DIR group (p = 0.031, p = 0.011, and p = 0.013, respectively). The total damage scores in the DIR-FC60 and DIR-S-FC60 groups were significantly lower than in the DIR group (p = 0.018 and p = 0.008, respectively). Furthermore, the levels of malondialdehyde (MDA) in the DIR-S, DIR-FC60, and DIR-S-FC60 groups were significantly lower than in the DIR group (p < 0.001, p < 0.001, and p < 0.001, respectively). Catalase (CAT) enzyme activity in the DIR-S, DIR-FC60, and DIR-S-FC60 groups was higher than in the DIR group (p = 0.001, p = 0.014, and p < 0.001, respectively). Superoxide dismutase (SOD) enzyme activity in the DIR-FC60 and DIR-S-FC60 groups was also higher than in the DIR group (p < 0.001 and p = 0.001, respectively). Conclusion: Our findings indicate that administering fullerenol C60 30 min prior to ischemia in diabetic mice, in combination with sevoflurane, led to a reduction in oxidative stress and the correction of IR-related damage in muscle tissue histopathology. We believe that the administration of fullerenol C60 before IR, coupled with sevoflurane administration during IR, exerts a protective effect in mice.

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Section: Discussionmentioning

confidence: 99%

Effects of sevoflurane and fullerenol C60 on lower limb ischemia–reperfusion injury in streptozocin-induced diabetic mice

Polat,

Şengel,

Küçük

et al. 2024

Science Progress

View full text Add to dashboard Cite

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“…For example, Salvia miltiorrhiza mitigates cardiac dysfunction and inflammation in rats with heart failure by inhibiting the formation of the MD2/TLR4-MyD88 complex [67]. Additionally, Astragaloside IV, Xiang Lin pills, berberine, and fluoxetine can inhibit the TLR4/MyD88/NF-κB signals, thereby exerting the effects of acute myocardial infarction, colitis, and ischemia-reperfusion injury, and relieve postoperative cognitive dysfunction and neuroinflammation in elderly mice [67][68][69][70][71][72][73][74][75][76][77][78][79][80]. Polyene phosphatidylcholine, a wellknown hepatoprotective drug, has also recently been found to act on the TLR2/MyD88 signaling pathway, inhibiting the binding of MyD88 and TLR, and activating the IκB kinase (IKK) complex to alleviate synovial inflammation [81].…”

Section: Drug Therapy Targeting Myd88mentioning

confidence: 99%

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

Song,

Li,

et al. 2024

Biomolecules

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The interplay between the immune system and cancer underscores the central role of immunotherapy in cancer treatment. In this context, the innate immune system plays a critical role in preventing tumor invasion. Myeloid differentiation factor 88 (MyD88) is crucial for innate immunity, and activation of MyD88 promotes the production of inflammatory cytokines and induces infiltration, polarization, and immune escape of immune cells in the tumor microenvironment. Additionally, abnormal MyD88 signaling induces tumor cell proliferation and metastasis, which are closely associated with poor prognosis. Therefore, MyD88 could serve as a novel tumor biomarker and is a promising target for cancer therapy. Current strategies targeting MyD88 including inhibition of signaling pathways and protein multimerization, have made substantial progress, especially in inflammatory diseases and chronic inflammation-induced cancers. However, the specific role of MyD88 in regulating tumor immunity and tumorigenic mechanisms remains unclear. Therefore, this review describes the involvement of MyD88 in tumor immune escape and disease therapy. In addition, classical and non-classical MyD88 inhibitors were collated to provide insights into potential cancer treatment strategies. Despite several challenges and complexities, targeting MyD88 is a promising avenue for improving cancer treatment and has the potential to revolutionize patient outcomes.

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Maternal nicotine exposure promotes hippocampal CeRNA-mediated excitotoxicity and social barriers in adolescent offspring mice

Zhao,

Li,

Cao

et al. 2024

Ecotoxicology and Environmental Safety

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Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway

Cited by 6 publications

References 57 publications

Effects of sevoflurane and fullerenol C60 on lower limb ischemia–reperfusion injury in streptozocin-induced diabetic mice

Effects of sevoflurane and fullerenol C60 on lower limb ischemia–reperfusion injury in streptozocin-induced diabetic mice

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

Maternal nicotine exposure promotes hippocampal CeRNA-mediated excitotoxicity and social barriers in adolescent offspring mice

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