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Diana Mao, MD presents at the 63rd annual meeting of the society for surgery of the alimentary tract

LSTAR Research Fellow Diana Mao, MD receives SSAT Resident Award

May 31, 2022, 16:57 PM by UTMB Surgery

LSTAR Research Fellow Diana Mao recently received a resident award at the 63rd annual meeting of the Society for Surgery of the Alimentary Tract (SSAT) in San Diego, California. Her abstract, titled: "Therapeutic Effect of Oridonin Against Inflammatory Bowel Disease Involves Inhibition of Intestinal Fibrosis Via NF-κB and P38/Stat1 Pathways" was created with Dr. Xiaofu Wang, Dr. Yanping Gu, and Dr. Ravi Radhakrishnan, all from UTMB. View more about her abstract below:

Intestinal fibrosis is a common sequela of inflammatory bowel disease (IBD) that may result in serious complications such as stricture and obstruction. In response to inflammatory stimuli, intestinal epithelial cells may undergo epithelial-mesenchymal transition (EMT), a process in which epithelial cells acquire a mesenchymal-like phenotype and participate in IBD-related fibrosis. Oridonin, a bioactive diterpenoid isolated from Rabdosia rubescens, has been reported to have therapeutic effects on IBD. However, the cellular mechanism remains unclear. We hypothesized that oridonin attenuates inflammation-related EMT and fibrogenesis in intestinal epithelial cells.

The rat intestinal epithelial cell line IEC-6 was exposed to lipopolysaccharide (LPS) after pretreatment with or without oridonin. Cellular protein levels were analyzed with Western blot or immunofluorescence assay.

Oridonin treatment suppressed LPS-induced activation of ?-smooth muscle actin (?-SMA), a marker of myofibroblasts, in IEC-6 cells. NF-?B was found to be an important regulator of ?-SMA. Oridonin inhibited LPS-induced NF-?B activation by blocking TNF?-induced NF-?B p65 nuclear translocation and DNA binding activity. TNF?-induced phosphorylation of IKK?/?, I?B?, and total I?B? degradation were inhibited by oridonin. Meanwhile, LPS-induced ?-SMA activation was found to be attenuated by the p38 specific inhibitor SB352085 but not by MEK/ERK or JNK inhibitors. Interestingly, oridonin did not affect LPS-stimulated p38 phosphorylation but significantly inhibited Stat1 activity, a downstream factor of p38. In addition, oridonin prevented LPS-stimulated fibronectin expression and restored LPS-inhibited tight junction protein ZO-1 expression in IEC-6 cells.

The anti-inflammatory effects of oridonin on intestinal epithelial cells may function by suppressing LPS-induced NF-?B and p38/Stat1 pathways and EMT-related fibrogenesis. Oridonin may be a promising drug candidate for IBD.


Congratulations, Dr. Mao!

Learn more about The Sealy & Smith Laboratory for Surgical Training, Assessment and Research (LSTAR) here

Learn more about the Society for Surgery of the Alimentary Tract (SSAT) here