The changes of oxidative stress and caspase-3 in swine with traumatic hemorrhagic shock in dry-heat environment of desert

Objective To study the changes of oxidative stress and caspase-3 in swine with traumatic hemorrhagic shock in dry-heat environment of desert. Methods A total of 48 Landrace small swine were randomly(random number)divided into 2 groups(n=24 in each group), and then the traumatic hemorrhagic shock was established in room temperature environment[(25±1)℃, (35±5)% humidity] and in dry-heat environment[(40.5±0.5)℃, (10±2)% humidity]in swine. Dry-heat environment traumatic hemorrhagic shock group (DHS), which was made in an artificial experiment cabin mimic the reality included swine exposed in the dry-heat environment of desert for 3 h (T0, n=6), T1 (50 min after shock modeling, n=6), T2 (100 min after shock modeling, n=6), T3 (150 min after shock modeling, n=6). At each interval, blood sample was collected to detect urea nitrogen (BUN) and creatinine, urine sample was collected to detect neutrophil gelatinase-associated lipoprotein (NGAL), kidney tissue samples were collected to evaluate renal morphological and tubular scores, as well as to detect catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA). Western blot was used to detect the level of caspase-3. Traumatic hemorrhagic shock group of room temperature environment (RTS) was established and variety of assays were carried out as same as those deteced in the dry-heat environment group. Results Compared with the room temperature environment exposed group, kidney damage index, antioxidant and caspase-3 were increased in desert dry-heat environment exposed for 3 h group, but there were no statistically significant difference(P> 0.05). And from T1 then on, the levels of NGAL, CAT and SOD in DHS groups were increased which were significant different from those in RTS group (P<0.05 or P<0.01). There were significant differences in BUN and creatinine at T2 between two groups(P<0.05). At T3, caspase-3 protein content in DHS group was significantly different from that in RTS group (P<0.01). Correlation analysis showed that the NGAL level was correlated with the levels to MDA (rRTS= 0.935, rDHS = 0.858, P<0.01) in RTS group and DHS group. Compared with RTS group, renal tissue under light microscope showed that Bowman appeared dilated with degeneration and exfoliated epithelial cells, proximal tubule epithelial shedding, and interstitial edema in DHS group. Electron microscope showed that mitochondria became pleomorphic, endoplasmic reticulum with fold broadening. Conclusions When traumatic hemorrhagic shock happened in the desert dry-heat environment, desert dry-heat environment can aggravate kidney damage, possibly by reducing the renal tissue antioxidant enzyme content and increase renal tissue caspase-3 activity to promote renal tissue apoptosis. Antioxidant stress and apoptosis may be an important role in the prevention of the secondary kidney injury induced by traumatic hemorrhagic shock in dry-heat environment. Key words: Desert; Dry-heat environment; Traumatic hemorrhagic shock; Oxidative stress; Apoptosis; Acute kidney injury