Figure 3 | Scientific Reports

Figure 3

From: Ischemia/reperfusion injured intestinal epithelial cells cause cortical neuron death by releasing exosomal microRNAs associated with apoptosis, necroptosis, and pyroptosis

Figure 3The alternative text for this image may have been generated using AI.

(A) Representative Western blots showing the expression levels of various parameters across experimental groups. β-actin was used as a loading control. (B) A representative immunoblot is shown, and bands of various parameters were quantified by densitometry and normalized to β-actin. (C) Bar graph quantifying the expression levels of cytokines in cortical neurons across experimental groups. (D) Bar graph quantifying the expression levels of extracellular IL-18 in co-culture media obtained from IEC-6 cells and primary cortical neurons. All measurements were made in triplicate, and each bar represents the mean ± S.D. *p < 0.05, compared with the Control Neuron+37 °C group; +p < 0.05, compared with the OGD-IEC-6+Neurons+37 °C group. (E) We hypothesize that the NLRP-1 inflammasome leads to caspase-1 activation and subsequent upregulation of proinflammatory cytokines such as IL-1β and IL-18, triggering pyroptosis, which ultimately induces HS pathology through several downstream effects in the brain. At the same time, apoptosis and necroptosis can also be observed. Our present data suggest that caspase-3-induced apoptosis, MLKL-induced necroptosis, and GSDMD-induced neuronal pyroptosis may provide a molecular basis for brain-gut interactions during HS. Hypothermia therapy may protect against HS by suppressing both the apoptosis, necroptosis and pyroptosis pathways.

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