Hypothermic machine perfusion (MP) can reduce graft's injury after kidney transplantation; however, the mechanism has not been elucidated. In the past decade, many studies showed that aldehyde dehydrogenase 2 (ALDH2) is a protease which can inhibit cell apoptosis. Therefore, this study aims to explore whether ALDH2 takes part in reducing organ damage after MP. Eighteen healthy male New Zealand rabbits (12 weeks old, weight 3.0 ± 0.3 kg) were randomly divided into three groups: normal group, MP group, and cold storage (CS) group (n = 6). The left kidney of rabbits underwent warm ischemia for 35 min through clamping the left renal pedicle and then reperfusion for 1 h. Left kidneys were preserved by MP or CS (4°C for 4 h) in vivo followed by the right nephrectomy and 24-h reperfusion, and then the specimens and blood were collected. Finally, concentration of urine creatinine (Cr), blood urea nitrogen (BUN), and 4-HNE were tested. Renal apoptosis was detected by TUNEL staining, and the expression of ALDH2, cleaved-caspase 3, bcl-2/ bax, MAPK in renal tissue was detected by immunohistochemistry or Western blot; 24 h after surgery, the concentration of Cr in MP group was 355 ± 71μmol/L, in CS group was 511 ± 44 μmol/L (P < 0.05), while the BUN was 15.02 ± 2.34 mmol/L in MP group, 22.64 ± 3.58 mmol/L in CS group (P < 0.05). The rate of apoptosis and expression of cleaved caspase-3, p-P38, p-ERK, and p-JNK in MP group was significantly lower than that in CS group (P < 0.05), while expression of ALDH2 and bcl-2/bax in MP group was significantly higher than that in CS group (P < 0.05); expression of cleaved caspase-3 in both MP and CS group significantly increased as compared with that in normal group (P < 0.05). In conclusion, increased expression of ALDH2 can reduce the renal cell apoptosis through inhibiting MAPK pathway during ischemia/reperfusion injury (IRI) after hypothermic MP.
Wound
healing is a clinical challenge, and nontoxic, nonadherent
wound dressings that promote healing are urgently needed. Herein,
hydroxybutyl chitosans (HBCSs) with the degree of substitution (DS)
from 0.41 to 1.38 were synthesized in alkali/urea aqueous solutions,
from which sponge-like dressings were prepared by freeze-drying. The
pore size of the sponges was in the range of 14.8–18.4 μm,
and the porosity was about 98–99%. The compressive strength
of the sponges decreased with increasing DS of HBCS. Cytocompatibility
studies with normal human dermal fibroblast (NHDF) cells demonstrated
that HBCSs were nontoxic and could even promote the growth of fibroblasts.
Further tests revealed that HBCS-3 (DS = 0.85) and HBCS-5 (DS = 1.38)
exhibited better hemocompatibility and a low blood-clotting index
(BCI). Therefore, these two samples were selected as model dressings
for in vivo wound-healing assessment in rats. The
experiments suggested that HBCS-3 significantly shortened the wound
recovery period compared with HBCS-5, chitosan, and gauze by facilitating
epithelialization, collagen deposition, and neovascularization and
activating the immune system. The results highlighted the potential
of HBCSs as efficient dressings for promoting wound healing.
Fibrous chitin dressing (FCD) prepared from a NaOH-urea aqueous solution of chitin via a physical process was used to study its effect on wound healing using a full-thickness cutaneous wound model in rats and mice.
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