Effects of propofol on damage of rat intestinal epithelial cells induced by heat stress and lipopolysaccharides

Abstract

Gut-derived endotoxin and pathogenic bacteria have been proposed as important causative factors of morbidity and death during heat stroke. However, it is still unclear what kind of damage is induced by heat stress. In this study, the rat intestinal epithelial cell line (IEC-6) was treated with heat stress or a combination of heat stress and lipopolysaccharide (LPS). In addition, propofol, which plays an important role in anti-inflammation and organ protection, was applied to study its effects on cellular viability and apoptosis. Heat stress, LPS, or heat stress combined with LPS stimulation can all cause intestinal epithelial cell damage, including early apoptosis and subsequent necrosis. However, propofol can alleviate injuries caused by heat stress, LPS, or the combination of heat stress and LPS. Interestingly, propofol can only mitigate LPS-induced intestinal epithelial cell apoptosis, and has no protective role in heat-stress-induced apoptosis. This study developed a model that can mimic the intestinal heat stress environment. It demonstrates the effects on intestinal epithelial cell damage, and indicated that propofol could be used as a therapeutic drug for the treatment of heat-stress-induced intestinal injuries.

Protective effects of baicalin on LPS-induced injury in intestinal epithelial cells and intercellular tight junctions

“…IL-6 and TNF-␣ are the critical cytokines involved in inflammation, and their inhibition is regarded as a common treatment strategy for inflammation-related diseases (Locksley et al 2001;Burger et al 2006). In this study, we used LPS at a concentration of 1.0 g/mL (Tang et al 2013) to establish the LPS-induced injury IEC-6 cell inflammation model. We first found that baicalin suppresses LPSinduced apoptosis in IEC-6 cells.…”

“…To date, 40 different proteins have been shown to be located in TJs, including, for example, ZO-1 proteins, occludin, and claudins (Liévin-Le and Servin 2006). Previous studies have shown that damage to IECs increases the permeability of the intestinal epithelial barrier, leading to an increase in gut-derived bacterial endotoxin translocation (Tang et al 2013) as a major factor contributing to the predisposition to inflammatory diseases of the bowel (Groschwitz and Hogan 2009) and bacteriainduced diarrhea (Hodges and Gill 2010). Lipopolysaccharide (LPS), a component of the outer wall of Gram-negative bacteria, induces the barrier function by activating chemical mediators (e.g., interleukin-6 (IL-6), tumor necrosis factor-␣ (TNF-␣), and nitric oxide), injuring epithelial cells and the TJs between epithelial cells (Hu et al 2013).…”

Chitooligosaccharides Attenuate Lipopolysaccharideinduced Inflammation and Apoptosis of Intestinal Epithelial Cells: Possible Involvement of TLR4/NF-κB Pathway.

“…8 Recognition of LPS by TLR4 leads to cellular activation and pro-inflammatory gene expression, the latter of which is thought to be responsible for the increase in apoptosis and damage in IECs observed in IBD. 8 Indeed, LPS was believed represent a robust, rapid and consistent stimulus for inducing pathological IEC apoptosis and inflammation, 5,9 thus would exacerbate the dysfunction of the epithelial barrier and further weaken the frontline defence against pathogenic bacteria. It is remarkable that IECs rather than macrophages or other lamina propria populations are found as the predominant cells expressing TLR4 in human intestinal mucosa.…”

α‐tocopherol decreases interleukin‐1β and ‐6 and increases human β‐defensin‐1 and ‐2 secretion in human gingival fibroblasts stimulated with Porphyromonas gingivalis lipopolysaccharide

“…This supports our study showing higher gingival fibroblast growth following stimulation with P. gingivalis LPS. This overgrowth may be a common cell behavior in response to endotoxin stimulation or possibly a cell‐specific behavior against the harmful effect of P. gingivalis or its virulence factors, thereby preventing periodontal disease . Interestingly, cell growth was promoted by α‐tocopherol, which suggests that this molecule may play a preventive role against periodontal disease.…”