Terazosin Stimulates Pgk1 to Remedy Gastrointestinal Disorders
Round 1
Reviewer 1 Report
This article studied the effect of terazosin, an α-adrenergic blocker, on ameliorating the DSS-induced ulcerative colitis and ethanol-induced gastric ulcer. The underlying mechanism of terazosin has also been investigated in this article. As an interesting finding, terazosin, which is used to treat hypertension, desired further study to explore its potential in treating gastrointestinal disorders alone or combining with other drugs.
Below are some minor suggestions about this article.
- Labeling the western blot graph with the group name will make the figures more intuitive.
- the states and protein level of Caco-2 cells will significantly change as the time of culture increases. Usually, the Caco-2 cannot mimic the intestinal mucosa well until 14-21 days. So, the authors can study the efficacy of terazosin by using the long-time cultured Caco-2.
- Do other α-adrenergic blockers show similar efficacy?
Author Response
Please see enclosure for details.
Author Response File: 
Author Response.pdf
Reviewer 2 Report
This study aimed to explore the anti-oxidation, anti-inflammation, anti-cell death properties of terazosin, an α-adrenergic receptor antagonist, in vivo and in vitro. The results demonstrate that terazosin exhibits anti-inflammatory effects by downregulating NF-κB-GSDMD signal pathway, along with enhancing glycolysis. Terazosin ameliorates ethanol-induced gastric mucosal damage in mice.
This study demonstrates for the first time that terazosin significantly activates Pgk1-mediated protective defenses against gastrointestinal disease
The research design is good, and the results of the experiment are clear. The results of this study provide clinically useful information
Author Response
Review #2: This study aimed to explore the anti-oxidation, anti-inflammation, anti-cell death properties of terazosin, an α-adrenergic receptor antagonist, in vivo and in vitro. The results demonstrate that terazosin exhibits anti-inflammatory effects by downregulating of NF-κB-GADMD signal pathway, along with enhancing glycolysis. Terazosin ameliorates ethanol-induced gastric mucosal damage in mice.
This study demonstrates for the first time that terazosin significantly activates Pgk1-mediated protective defense against gastrointestinal disease.
The research design is good, and the results of the experiment are clear. The results of this study provide clinically useful information.
Response: Thank you for your kind recognition of our work.
