TY - JOUR
T1 - Nitric Oxide Modulation as a Potential Molecular Mechanism Underlying the Protective Role of NaHS in Liver Ischemia Reperfusion Injury
AU - Ibrahim, Salwa A.
AU - Abdel-Gaber, Seham A.
AU - Ibrahim, Mohamed A.
AU - Amin, Entesar F.
AU - Mohammed, Rehab K.
AU - Abdelrahman, Aly M.
N1 - Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
PY - 2022/7/1
Y1 - 2022/7/1
N2 - 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 TN-F-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. © 2022 Bentham Science Publishers.
AB - 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 TN-F-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. © 2022 Bentham Science Publishers.
KW - Ischemia reperfusion injury
KW - hepatic surgery
KW - liver cells
KW - nitric oxide
KW - sodium hydrosulfide
KW - transplantation
KW - Antioxidants/pharmacology
KW - Rats
KW - Male
KW - Nitric Oxide
KW - Reperfusion Injury/drug therapy
KW - Tumor Necrosis Factor-alpha
KW - Liver/pathology
KW - Sulfides
KW - Animals
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UR - https://www.mendeley.com/catalogue/775f5aaf-a431-3b5a-8568-c1df601eac5f/
U2 - 10.2174/1874467214666210909154609
DO - 10.2174/1874467214666210909154609
M3 - Article
C2 - 34503437
AN - SCOPUS:85118763578
SN - 1874-4672
VL - 15
SP - 676
EP - 682
JO - Current Molecular Pharmacology
JF - Current Molecular Pharmacology
IS - 4
ER -