Published online Mar 21, 2020. doi: 10.3748/wjg.v26.i11.1156
Peer-review started: November 12, 2019
First decision: December 23, 2019
Revised: December 27, 2019
Accepted: February 21, 2020
Article in press: February 21, 2020
Published online: March 21, 2020
Intestinal inflammation is a common digestive tract disease at present, which is usually treated with hormone medications. Hormone medications are effective to some extent, but long-term use of them may bring about many complications. Therefore, it is very important to find new drugs to treat intestinal inflammation.
Panax notoginseng saponins (PNS) are a class of drugs widely used in cardiovascular diseases and diabetes, which have been proven to have good inflammatory inhibition effects. However, there are few studies on the role and mechanism of PNS in rat models of intestinal inflammation. PNS may be an effective drug for intestinal inflammation.
This study aimed to explore the effects of PNS on dextran sulfate sodium (DSS)-induced intestinal inflammatory injury in rats, and its possible mechanism.
The colitis rat models were constructed by inducing DSS, and treating with different concentrations of PNS to inhibit the phosphoinositide-3-kinase protein kinase B (PI3K/AKT) signaling pathway in colon tissues. Then the intestinal injury, oxidative stress parameters, inflammatory indices, tight junction proteins, apoptosis, macrophage polarization, and PI3K/AKT signaling were detected in the tissues.
Compared with colitis rats, rats intervened with PNS showed significantly lengthened colons, decreased disease activity index, as well as significantly alleviated oxidative stress reactions and inflammatory responses. Furthermore, they showed significantly increased expression of tight junction-associated proteins, significantly decreased apoptotic cells, significantly decreased M1 macrophages in spleen and colon tissues, and significantly increased M2 macrophages in colon tissues. They also showed significantly suppressed activation of the PI3K /AKT signaling pathway, and dose-dependency. When the PI3K/AKT signaling pathway was inhibited, compared with colitis rats, the apoptosis rate of colon tissue treated with LY294002 decreased significantly.
This study confirmed that PNS can protect rats against DSS-induced intestinal inflammatory injury by inhibiting the PI3K/AKT signaling pathway, and revealed that it may have potential to be used in the future as a drug for colitis.
It has been proven that PNS can play a protective role against intestinal injury in colitis rats by inhibiting the PI3K/AKT signaling pathway, and PNS may be a potential effective drug for treating colitis.