Reviewer's report
Title:Carbon monoxide-Releasing Molecule-2 (CORM-2) attenuates acute
hepatic ischemia reperfusion injury in rats
Version: 1Date:19 January 2010
Reviewer: Bingwei Sun
Reviewer's report:
Major Compulsory Revisions.
The manuscript by Yunwei Wei, et al. entitled “Carbon monoxide-Releasing
Molecule-2 (CORM-2) attenuates acute hepatic ischemia reperfusion injury in
rats” is presented for review.
The obtained results indicate that CORM-2-released CO protected the liver from
I/Ri by a reduction of AST and ALT, upregulated the expression of Bcl-2 protein,
inhibited the activation of NF-#B, reduced the cytokines production, and
attenuated the PMN accumulation in the liver after I/Ri.
The proposed experiments are straightforward and well controlled. The findingsof
the present study seems interesting, however, the major concern with the
manuscript is the dose of CORM-2 administrated in this study. The CORM-2
concentration used in the current study (i.e. 8mg/ml) was originally described and
used in mouse model of sepsis (Sun BW, et al. “Attenuation of Leukocytes
Sequestration by CO-releasing Molecules -liberated CO in the Liver of Thermal
Mice” J Burn Care Res. 2007#28#1##173-181 and Cepinskas et al. “Carbon
monoxide liberated from carbon monoxide-releasing molecule CORM-2
attenuates inflammation in the liver of septic mice” Am J Physiol Gastrointest
Liver Physiol 294: G184–G191, 2008). However, why the authors used the same
dose of CORM-2 for the study in rats? Did the authors measure the COHb level
in the rats under the administration of CORM-2 with the dose of 8mg/ml?
This issue should be properly addressed.
Additional points to consider:
1. Carbon monoxide (CO) is well known to have anti-inflammatory, anti-oxidative
and cytoprotective effects. In this study, the authors observed the
anti-inflammatory effects of CO in the liver I/R model in rats. However, they did
not rule out the effects of other products (i.e. bilirubin) of HO-1 activity. Therefore,
it is necessary to use HO-1 inhibitor to know pure effects of CO in the liver I/R
model in rats.
2. Abstract Results, line 7: should be “….of the adhesion molecule ICAM-1 in the
endothelial cells of liver.”
3. Materials and methods section: liver NF-#B activation:15mg protein was used?
4. Why the authors design the time point of CORM-2 treatment at the time of
reperfusion, not at the time of ischemia?
5. Ref. 25: incomplete reference.
Level of interest: An article of limited interest
Quality of written English: Needs some language corrections before being
published
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Declaration of competing interests:
I declare that I have no competing interests.
Reviewer's report
Title:Carbon monoxide-Releasing Molecule-2 (CORM-2) attenuates acute
hepatic ischemia reperfusion injury in rats
Version: 1Date:19 January 2010
Reviewer: Bingwei Sun
Reviewer's report:
Major Compulsory Revisions.
The manuscript by Yunwei Wei, et al. entitled “Carbon monoxide-Releasing
Molecule-2 (CORM-2) attenuates acute hepatic ischemia reperfusion injury in
rats” is presented for review.
The obtained results indicate that CORM-2-released CO protected the liver from
I/Ri by a reduction of AST and ALT, upregulated the expression of Bcl-2 protein,
inhibited the activation of NF-#B, reduced the cytokines production, and
attenuated the PMN accumulation in the liver after I/Ri.
The proposed experiments are straightforward and well controlled. The findingsof
the present study seems interesting, however, the major concern with the
manuscript is the dose of CORM-2 administrated in this study. The CORM-2
concentration used in the current study (i.e. 8mg/ml) was originally described and
used in mouse model of sepsis (Sun BW, et al. “Attenuation of Leukocytes
Sequestration by CO-releasing Molecules -liberated CO in the Liver of Thermal
Mice” J Burn Care Res. 2007#28#1##173-181 and Cepinskas et al. “Carbon
monoxide liberated from carbon monoxide-releasing molecule CORM-2
attenuates inflammation in the liver of septic mice” Am J Physiol Gastrointest
Liver Physiol 294: G184–G191, 2008). However, why the authors used the same
dose of CORM-2 for the study in rats? Did the authors measure the COHb level
in the rats under the administration of CORM-2 with the dose of 8mg/ml?
This issue should be properly addressed.
Additional points to consider:
1. Carbon monoxide (CO) is well known to have anti-inflammatory, anti-oxidative
and cytoprotective effects. In this study, the authors observed the
anti-inflammatory effects of CO in the liver I/R model in rats. However, they did
not rule out the effects of other products (i.e. bilirubin) of HO-1 activity. Therefore,
it is necessary to use HO-1 inhibitor to know pure effects of CO in the liver I/R
model in rats.
2. Abstract Results, line 7: should be “….of the adhesion molecule ICAM-1 in the
endothelial cells of liver.”
3. Materials and methods section: liver NF-#B activation:15mg protein was used?
4. Why the authors design the time point of CORM-2 treatment at the time of
reperfusion, not at the time of ischemia?
5. Ref. 25: incomplete reference.
Level of interest: An article of limited interest
Quality of written English: Needs some language corrections before being
published
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Declaration of competing interests:
I declare that I have no competing interests.
Please review this paper.
user
Reviewer's report
Title:Carbon monoxide-Releasing Molecule-2 (CORM-2) attenuates acute
hepatic ischemia reperfusion injury in rats
Version: 1Date:19 January 2010
Reviewer: Bingwei Sun
Reviewer's report:
Major Compulsory Revisions.
The manuscript by Yunwei Wei, et al. entitled “Carbon monoxide-Releasing
Molecule-2 (CORM-2) attenuates acute hepatic ischemia reperfusion injury in
rats” is presented for review.
The obtained results indicate that CORM-2-released CO protected the liver from
I/Ri by a reduction of AST and ALT, upregulated the expression of Bcl-2 protein,
inhibited the activation of NF-#B, reduced the cytokines production, and
attenuated the PMN accumulation in the liver after I/Ri.
The proposed experiments are straightforward and well controlled. The findingsof
the present study seems interesting, however, the major concern with the
manuscript is the dose of CORM-2 administrated in this study. The CORM-2
concentration used in the current study (i.e. 8mg/ml) was originally described and
used in mouse model of sepsis (Sun BW, et al. “Attenuation of Leukocytes
Sequestration by CO-releasing Molecules -liberated CO in the Liver of Thermal
Mice” J Burn Care Res. 2007#28#1##173-181 and Cepinskas et al. “Carbon
monoxide liberated from carbon monoxide-releasing molecule CORM-2
attenuates inflammation in the liver of septic mice” Am J Physiol Gastrointest
Liver Physiol 294: G184–G191, 2008). However, why the authors used the same
dose of CORM-2 for the study in rats? Did the authors measure the COHb level
in the rats under the administration of CORM-2 with the dose of 8mg/ml?
This issue should be properly addressed.
Additional points to consider:
1. Carbon monoxide (CO) is well known to have anti-inflammatory, anti-oxidative
and cytoprotective effects. In this study, the authors observed the
anti-inflammatory effects of CO in the liver I/R model in rats. However, they did
not rule out the effects of other products (i.e. bilirubin) of HO-1 activity. Therefore,
it is necessary to use HO-1 inhibitor to know pure effects of CO in the liver I/R
model in rats.
2. Abstract Results, line 7: should be “….of the adhesion molecule ICAM-1 in the
endothelial cells of liver.”
3. Materials and methods section: liver NF-#B activation:15mg protein was used?
4. Why the authors design the time point of CORM-2 treatment at the time of
reperfusion, not at the time of ischemia?
5. Ref. 25: incomplete reference.
Level of interest: An article of limited interest
Quality of written English: Needs some language corrections before being
published
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Declaration of competing interests:
I declare that I have no competing interests.
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