Danhong Injection Alleviates Postoperative Intra-abdominal Adhesion in a Rat Model

Abstract

Background. Among all the common complications that occur after abdominal surgery, intestinal adhesion is perhaps the most unpleasant one. However, current methods to treat and prevent intestinal adhesion are limited; thus, exploring new methods to prevent and treat intestinal adhesion is greatly needed. In this study, we demonstrated that Danhong injection (DHI) may be used as a promising method to prevent and treat intra-abdominal adhesion in a rat model. Materials and Methods. Forty-eight rats were randomly divided into six groups. Except for the sham-operated group, all rats underwent cecal abrasion to establish an adhesion model. After the operation, the rats in the DHI-treated groups received different doses of DHI via the tail vein daily, while the other group was treated with the same volume of saline solution. Seven days after the operation, all rats were sacrificed, and the degree of adhesion was evaluated by Nair’s scoring system. The extent of inflammation in the adhesion tissue was detected by HE staining and the expression of tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β). The collagen deposition was assessed by Sirius red staining and α-SMA, MMP9, t-PA, and PAI-1 levels. Oxidative stress was indicated by the level of reactive oxygen species (ROS) in adhesion tissues and by immunohistochemical labeling of Nrf2. Furthermore, rat primary peritoneal mesothelial cells (RPMCs) were treated with H2O2 and DHI, and NF-κB phosphorylation was detected to illustrate the effect of DHI on oxidative stress. Results. The intra-abdominal adhesion scores were significantly decreased in the groups treated with a high dose of DHI compared with the control groups, and the degree of inflammation, fibrosis, and oxidative stress was also significantly decreased. DHI treatment significantly reduced the levels of TNF-α, TGF-β1, and PAI and increased the expression levels of MMP9, Nrf2, and t-PA in the adhesion tissues. ROS levels and NF-κB phosphorylation were significantly reduced in DHI-treated RPMCs compared with the control RPMCs. Conclusion. DHI alleviates the formation of postoperative intra-abdominal adhesions by inhibiting inflammation, collagen deposition, and oxidative stress in a rat model and may serve as a promising drug to prevent intra-abdominal adhesions.

Adipose Mesenchymal Stem Cell-Derived Exosomes Relieve Postoperative Abdominal Adhesion By Activating the MAPK-ERK 1/2 and PI3K-Akt Pathways

“…In addition, the levels of α-SMA and bronectin were also detected, which displayed a decreasing trend. Previous evidences showed that over-expression of α-SMA and bronectin inhibitors prevented postoperative scaring and brosis development after PAs [40,41]. In conclusion, our ndings indicate that ADSC-Exos critically suppresses development of peritoneal adhesions and accelerates the rapid healing of mesenchymal cells after peritoneal injury.…”

TMIGD1 Inhibited Abdominal Adhesion Formation by Alleviating Oxidative Stress in the Mitochondria of Peritoneal Mesothelial Cells

“…A series of pictures were taken using a Nikon Eclipse C1 confocal laser scanning microscope (Nikon Corporation, Tokyo, Japan). The assessment IHC was performed as reported previously [ 18 ], and at least five fields were selected for every section. The scoring system was as follows: a score of 0 indicated tissues with no expression, a score of 1 indicated tissue with weakly positive expression, a score of 2 indicated tissues with positive expression, a score of 3 indicated tissues with strongly positive expression, and a score of 4 indicated tissues with extremely abundant expression.…”

Analysis on clinical association of uterine scar diverticulum with subsequent infertility in patients underwent cesarean section

“…[ 22 ] TNF-α is recognized as a marker for the formation of intra-abdominal adhesion, which can promote local inflammation of tissues, and leading to the development of tissue fibrosis. [ 23 ] Current study has found that IL-1β and TNF-α are strong inducers of IL-6, and the high concentration of IL-6 in serum is a risk factor for tubal factor infertility. [ 24 ] Additionally, we evaluated the correlation between cytokines and infertility, and the results indicated that the contents of cytokines were positively correlated with subsequent infertility.…”