Induction of Heat Shock Response: Effect on the Rat Liver with Carbon Tetrachloride‐induced Fibrosis from Ischemia‐reperfusion Injury

Abstract

The role of heat shock pretreatment in the induction of tolerance for ischemia-reperfusion injury was investigated in rat livers with fibrosis produced by carbon tetrachloride (CCI4) injected subcutaneously. The control group (group C, n = 56) received no pretreatment except anesthesia, and the heat shock group (group HS, n = 56) were exposed to heat shock (42 degrees C) for 15 minutes. After a 48-hour recovery all rats were subjected to 30 minutes of warm ischemia. Western blotting analysis was employed for heat shock protein (HSP) 72 detection. The adenine nucleotide levels in liver tissue and the liver enzyme levels in serum were measured before and after ischemic intervention (seven animals were used at each of six time point measurements in both groups). HSP72 was induced in group HS at greater intensity than in group C. The survival rate on postoperative day 7 in group C (3/14) was significantly poorer than that in group HS (14/14) (p < 0.01). The higher survival rate in group HS was accompanied by more rapid recovery of the adenosine triphosphate level and lower serum levels of liver enzymes after reperfusion (p < 0.01 vs. group C). Heat shock preconditioning induces HSP72 in the rat liver with fibrosis and provides significantly increased tolerance of warm-ischemia reperfusion injury.

The Hepatic Microcirculation: Mechanistic Contributions and Therapeutic Targets in Liver Injury and Repair

“…These include the application of adenosine (724), adenosine A(1) and A(2) receptor agonists (9,19,451), as well as nitrite (NO 2Ϫ ) as an intrinsic signaling molecule that is reduced to NO (738) and bilirubin as metabolite of the HO-1 metabolism (372). However, protection can also be achieved by induction of heat shock (558,733), infusion of gluthatione (706), or exposure to ozone (10,478) and hyperbaric oxygen (945).…”

Advantage of Ischemic Preconditioning for Hepatic Resection in Pigs

“…A cirrhotic liver is more vulnerable to ischemia than a liver with normal parenchyma, and prolonged ischemia increased morbidity after hepatic resection [36]. Only a few reports investigated whether IP can prevent aggravation of I/R injury in cirrhotic parenchyma [37]. Thus, at this moment, in clinical hepatic resection, if the total ischemic time is supposed to be within 60 min in normal liver parenchyma, IP might be the best option for hepatic parenchymal resection, because most hepatic resection can be conducted within 60 min under continuous inflow occlusion without increased morbidities.…”

A hősokkfehérjék hatása a máj ischaemiás-reperfúziós károsodására

“…A HSP72 gén transzkripciójának indukciója az inflammátoros citokinek transzkripciójának gátlásá-hoz vezethet [29]. A fehérje különféle stressz által kivál-tott ingerek hatására képződik, és fontos szerepet tulajdonítanak neki a sejt homeosztázisának fenntartásában és ezáltal a betegek túlélési esélyeinek növelésében [30]. Az intracelluláris térben a HPS72 az inflammátoros citokinek negatív szabályozásában játszhat szerepet, megelőzve a túlságosan magas inflammátoroscitokin-szintet a sejten belül, ami a gyulladás során a sejt véletlenszerű károsodásához vagy halálához vezethet [31].…”