Nitric Oxide Modulation as a Potential Molecular Mechanism Underlying the Protective Role of NaHS in Liver Ischemia Reperfusion Injury / Salwa A. Ibrahim, Seham A. Abdel-Gaber, Mohamed A. Ibrahim, Entesar F. Amin, Rehab K. Mohammed, Aly M. Abdelrahman
Background: Liver IR is a frequent clinical complication with high morbidity and mortality. The present study evaluated the possible protective effect of sodium hydrosulfide (NaHS), a H2S donor, in IR-induced hepatic injury and explored the mechanisms of actions of the investigated drug. Methods: Male albino rats (200-230 g) were divided into the following groups: group 1:Sham-operated non treated rats, group 2: IR non treated rats, group 3: L-NNA + IR rats, group 4: NaHS + IR rats, group 5: L-NNA + NaHS + IR rats. Blood samples were collected for ALT determination. Liver tissue samples were used for the assessment of GPx, catalase, SOD, MDA, total nitrites and TNF- α. Parts from the liver were fixed in 10% formalin solution for histopathological examination and immunohistochemical examination of iNOS, eNOS and caspase-3. Results: NaHS protected the liver against IR. This hepatoprotection was associated with normalization of antioxidant enzyme activity and decrease in hepatic MDA, TNF-α and expression of caspase- 3 and iNOS. Conclusion: NaHS is hepatoprotective in IR injury. The hepatoprotective effects of NaHS are associated with antioxidant, anti-inflammatory and antiapoptotic effects. These effects are probably mediated via NO modulation.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2022 |
---|---|
Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - volume:15 |
---|---|
Enthalten in: |
Current molecular pharmacology - 15(2022), 4, Seite 7 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Ibrahim, Salwa A. [VerfasserIn] |
---|
Links: |
FID Access [lizenzpflichtig] |
---|
Umfang: |
1 Online-Ressource (7 p) |
---|
Förderinstitution / Projekttitel: |
|
---|
PPN (Katalog-ID): |
KFL011168498 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | KFL011168498 | ||
003 | DE-627 | ||
005 | 20231128145904.0 | ||
007 | cr uuu---uuuuu | ||
008 | 230613s2022 xx |||||o 00| ||eng c | ||
035 | |a (DE-627)KFL011168498 | ||
035 | |a (KFL)prod_DARH_.5DB0139BEB2CCC7375B792ABC35CD2F2D94A91C5 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
084 | |a PHARM |q DE-84 |2 fid | ||
100 | 1 | |a Ibrahim, Salwa A. |e verfasserin |4 aut | |
245 | 1 | 0 | |a Nitric Oxide Modulation as a Potential Molecular Mechanism Underlying the Protective Role of NaHS in Liver Ischemia Reperfusion Injury |c Salwa A. Ibrahim, Seham A. Abdel-Gaber, Mohamed A. Ibrahim, Entesar F. Amin, Rehab K. Mohammed, Aly M. Abdelrahman |
264 | 1 | |c 2022 | |
300 | |a 1 Online-Ressource (7 p) | ||
336 | |a Text |b txt |2 rdacontent | ||
337 | |a Computermedien |b c |2 rdamedia | ||
338 | |a Online-Ressource |b cr |2 rdacarrier | ||
520 | |a Background: Liver IR is a frequent clinical complication with high morbidity and mortality. The present study evaluated the possible protective effect of sodium hydrosulfide (NaHS), a H2S donor, in IR-induced hepatic injury and explored the mechanisms of actions of the investigated drug. Methods: Male albino rats (200-230 g) were divided into the following groups: group 1:Sham-operated non treated rats, group 2: IR non treated rats, group 3: L-NNA + IR rats, group 4: NaHS + IR rats, group 5: L-NNA + NaHS + IR rats. Blood samples were collected for ALT determination. Liver tissue samples were used for the assessment of GPx, catalase, SOD, MDA, total nitrites and TNF- α. Parts from the liver were fixed in 10% formalin solution for histopathological examination and immunohistochemical examination of iNOS, eNOS and caspase-3. Results: NaHS protected the liver against IR. This hepatoprotection was associated with normalization of antioxidant enzyme activity and decrease in hepatic MDA, TNF-α and expression of caspase- 3 and iNOS. Conclusion: NaHS is hepatoprotective in IR injury. The hepatoprotective effects of NaHS are associated with antioxidant, anti-inflammatory and antiapoptotic effects. These effects are probably mediated via NO modulation | ||
700 | 1 | |a Abdel-Gaber, Seham A. |e verfasserin |4 aut | |
700 | 1 | |a Ibrahim, Mohamed A. |e verfasserin |4 aut | |
700 | 1 | |a Amin, Entesar F. |e verfasserin |4 aut | |
700 | 1 | |a Mohammed, Rehab K. |e verfasserin |4 aut | |
700 | 1 | |a Abdelrahman, Aly M. |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Current molecular pharmacology |d Sharjah : Bentham, 2008 |g 15(2022), 4, Seite 7 |h Online-Ressource |w (DE-627)KFL000006564 |w (DE-600)2433118-1 |w (DE-576)306836815 |x 1874-4702 |7 nnns |
773 | 1 | 8 | |g volume:15 |g year:2022 |g number:4 |g pages:7 |
856 | 4 | 0 | |u http://pharmazie.proxy.fid-lizenzen.de/fid/bentham-ejournals-pharmazie/www.eurekaselect.com/openurl/content.php?genre=article&issn=1874-4672&volume=15&issue=4&spage=676 |m X:KFL |x Verlag |y FID Access |z lizenzpflichtig |
912 | |a ZDB-1-BEJ | ||
912 | |a GBV_KFL | ||
912 | |a FID-PHARM | ||
935 | |i IMPORT_0628_prod_DARH_03 | ||
951 | |a AR | ||
952 | |d 15 |j 2022 |e 4 |h 7 |