scholarly journals Abscisic Acid Can Protect the Kidney Against Ischemia/Reperfusion Injury Via Antiapoptotic Activity, Downregulation of NOX-4 and Upregulation of Connexin-43

2021 ◽  
Vol 41 (4) ◽  
pp. 537-552
Author(s):  
Mohamed Adel ◽  
Mohammed Rabei ◽  
Noha Hazem ◽  
Hassan Reda Hassan Elsayed ◽  
Mohammad El-Nablawy
2021 ◽  

Background: Ischemia-reperfusion injury (IRI) is an injurious phenomenon that is the primary determinant of liver dysfunction after surgery and transplantation. The present evidence demonstrated that connexin 43 (Cx43), Cx32, and Cx26 are the essential gap junction proteins involved in the liver IRI. This study aimed to characterize the beneficial effects of silibinin on Cx43, Cx32, and Cx26 gene expression during warm hepatic ischemia-reperfusion (IR). Materials and Methods: A total of 32 male Wistar rats weighing 250-300 g were randomly divided into four equal groups of eight animals in each group as follows: 1) control group (laparotomy+normal saline), 2) laparotomy+silibinin (30 mg/kg) (SILI), 3) liver IR procedure+normal saline (IR), and 4) liver IR procedure+silibinin (30 mg/kg) (IR+SILI). After 1 h of ischemia followed by 3 h of reperfusion, blood samples and tissue sections were gathered to assess the serum liver markers and evaluate the liver histological changes as well as gene expression, respectively. Results: The obtained data proved no considerable differences between control and SILI groups in all experiments. Furthermore, the gene expression of Cx26, Cx32, and Cx43 was significantly induced in the IR group, compared to the control group. Silibinin markedly reduced Cx26 and Cx32 mRNA expression, whereas increased Cx43 mRNA expression. Moreover, serum alanine aminotransferase and aspartate aminotransferase levels were markedly elevated in the IR group (P<0.001), compared to the control group. However, in the IR+SILI group, silibinin could significantly decline these elevations, compared to the IR group. In addition, silibinin diminished hepatic tissue damages during IR. Conclusion: Silibinin could attenuate liver injury through better cell-to-cell communication via lowering Cx32 and Cx26, as well as increasing Cx43 gene expression, respectively.


2005 ◽  
pp. 31-32
Author(s):  
Antonio Rodriguez-Sinovas ◽  
David García-Dorado ◽  
Alberto Cabestrero ◽  
Marisol Ruiz-Meana

2015 ◽  
Vol 153 ◽  
pp. 90-106 ◽  
Author(s):  
Rainer Schulz ◽  
Philipp Maximilian Görge ◽  
Anikó Görbe ◽  
Péter Ferdinandy ◽  
Paul D. Lampe ◽  
...  

2007 ◽  
Vol 293 (3) ◽  
pp. H1714-H1720 ◽  
Author(s):  
Kaori Shintani-Ishida ◽  
Koichi Uemura ◽  
Ken-ichi Yoshida

The aim of this study was to investigate changes in hemichannel activity during in vitro simulated ischemia [oxygen-glucose deprivation (OGD)] and the contribution of hemichannels to ischemia-reperfusion injury in rat neonatal cardiomyocytes. Dye uptake assays showed that hemichannels opened as OGD progressed, peaking after 1 h, and then closed, returning to the pre-OGD state after 2 h of OGD. The increase in dye uptake after 1 h of OGD was inhibited by hemichannel blockers (lanthanum chloride and a connexin 43 mimetic peptide, Gap26). During OGD, intracellular Ca2+ concentration ([Ca2+]i) began to increase after 1 h and reached several micromolar after 2 h. After 1 h of OGD, Gap26 inhibited the increases in hemichannel activity and [Ca2+]i. In contrast, dantrolene [an endo(sarco)plasmic reticulum Ca2+ release inhibitor] suppressed the increase in [Ca2+]i, but not in hemichannel activity. After 2 h of OGD, the combined administration of 2′,4′-dichlorobenzamil and dantrolene reduced [Ca2+]i to <1 μM and increased hemichannel activity to the level attained after 1 h of OGD. Simulated ischemia-reperfusion, induced by 1 h of OGD followed by 2 h of recovery, reduced cell viability to 54% of the control level. The addition of Gap26 to OGD medium improved viability to 80% of the control level. In conclusion, this study demonstrated that 1) hemichannels open transiently during OGD, 2) closure of hemichannels, but not their opening, is regulated by an increase in [Ca2+]i during OGD, and 3) open hemichannels contribute to cell injury during recovery from OGD.


Sign in / Sign up

Export Citation Format

Share Document