Page 219 - 2014 Printable Abstract Book
P. 219
Furthermore, the administration with SNP achieved not only the suppression of apoptosis of cells
distributed at the bottom of the intestinal crypts on Day 2 but also the recuperation of the bone marrow
stem and progenitor cells on Day 14. These results indicate a possibility of SNP as a first-aid medicine for
emergency acute exposure to radiation.
(PS3-52) Acute Intestinal Injury of Mice Induced by Whole Body Irradiation and Treated by
Peptidoglycan and Amifostine. Jianping Cao, Ph.D; Soochow University, Suzhou, China
Objective: Peptidoglycan (PGN), an agonist of TLR2, has radioprotective activity, while amifostine
(WR2721) has the effects on eliminating free radicals induced by irradiation. The objective of this study
was to evaluate the treatment affect of PGN and ER2721 on the acute intestinal injury of mice induced by
WBI. Methods: Six- to eight-week-old C57BL/6 mice were whole body exposed to a single dose of 15Gy X-
rays (Philips SL18, 200cGy/min). The features of apoptotic, necrosis and autophagical in ileums of mice
were observed by transmission electron micrographs (TEM) and the biochemical features. 150mg/kg of
WR2721 and PGN were administrated by intraperitoneal injection 30 minutes pre and 24hrs after
irradiation, respectively.Results: (1) 15Gy whole body irradiation (WBI) is lethal to mice. Most mice only
survived for 4 days after 15Gy WBI and had almost 20% body weight loss at day 3 after 15Gy WBI. (2) At
3.5 days post-WBI, there was serious gastrointestinal (GI) pathological damage: decrease significantly in
stool number and villous length compared with normal mice. (3) The lever of reactive oxygen species
(ROS) in ileums increased obviously after irradiation, but the oxidation index (GSH, NO, H2O2, SOD) did
not change obviously. (4) The presence of cleaved caspase 3 (apoptosis marker), the conversion from light
chain 3 (LC3)-I to LC3-II (autophage marker), the secretion of interleukin (IL)6 in serum and the expression
and secretion of high mobility group box chromosomal protein (HMGB)1 (necrosis) was induced after
irradiation. (5) Acetylation of Tp53 at lysine 379 and phosphorylation of Tp53 at serine 6/20/392 could be
induced after 15Gy and disappeared at 2 hrs after WBI. (6) 50% mice treated with PGN and WR2721
unitedly could live more than 30 days, while the mice treated with PGN and WR2721 alone died in 9 days
after WBI, and the mice untreated could live less than 5 days after WBI (p<0.01). Conclusions: WBI at a
single dose of 15Gy X-rays would induce GI syndrome, which manifested by less stool formation and lower
body weight with the time post irradiation. At the 5th day after 15Gy WBI, all mice were died. The intestine
cells’ death couldn’t be classified into one kind of death but belonged to “mixed death”. The treatment
effect of PGN and WR2721 unitedly on the WBI mice is better than PGN or WR2721 alone.
(PS3-53) The mechanism and treatment for radiation-induced skin injury: intensification of
antioxidant capability. Shuyu Zhang, Soochow University, Suzhou, China
Ionizing radiation is used extensively to treat many different types of cancer and contributes to
40% of curative cancer treatments. However, radiotherapy may significantly injure the skin and
profoundly impair its function. Radiation-induced skin injury is a serious concern that may limit the
duration and the delivered dose of radiation. However, the molecular mechanism underlying the
pathogenesis of radiation-induced skin injury is largely unknown. Using miRNA microarray, we found that
many miRNAs were significantly dysregulated in irradiated skin tissues, including miR-223, miR-21 and
miR-34a.Using 2-DE and MS, we identified 24 proteins in rat skin tissues irradiated with 45 Gy of electron
beam. These identified differentially expressed proteins included mitochondrial aspartate
217 | P a g e
distributed at the bottom of the intestinal crypts on Day 2 but also the recuperation of the bone marrow
stem and progenitor cells on Day 14. These results indicate a possibility of SNP as a first-aid medicine for
emergency acute exposure to radiation.
(PS3-52) Acute Intestinal Injury of Mice Induced by Whole Body Irradiation and Treated by
Peptidoglycan and Amifostine. Jianping Cao, Ph.D; Soochow University, Suzhou, China
Objective: Peptidoglycan (PGN), an agonist of TLR2, has radioprotective activity, while amifostine
(WR2721) has the effects on eliminating free radicals induced by irradiation. The objective of this study
was to evaluate the treatment affect of PGN and ER2721 on the acute intestinal injury of mice induced by
WBI. Methods: Six- to eight-week-old C57BL/6 mice were whole body exposed to a single dose of 15Gy X-
rays (Philips SL18, 200cGy/min). The features of apoptotic, necrosis and autophagical in ileums of mice
were observed by transmission electron micrographs (TEM) and the biochemical features. 150mg/kg of
WR2721 and PGN were administrated by intraperitoneal injection 30 minutes pre and 24hrs after
irradiation, respectively.Results: (1) 15Gy whole body irradiation (WBI) is lethal to mice. Most mice only
survived for 4 days after 15Gy WBI and had almost 20% body weight loss at day 3 after 15Gy WBI. (2) At
3.5 days post-WBI, there was serious gastrointestinal (GI) pathological damage: decrease significantly in
stool number and villous length compared with normal mice. (3) The lever of reactive oxygen species
(ROS) in ileums increased obviously after irradiation, but the oxidation index (GSH, NO, H2O2, SOD) did
not change obviously. (4) The presence of cleaved caspase 3 (apoptosis marker), the conversion from light
chain 3 (LC3)-I to LC3-II (autophage marker), the secretion of interleukin (IL)6 in serum and the expression
and secretion of high mobility group box chromosomal protein (HMGB)1 (necrosis) was induced after
irradiation. (5) Acetylation of Tp53 at lysine 379 and phosphorylation of Tp53 at serine 6/20/392 could be
induced after 15Gy and disappeared at 2 hrs after WBI. (6) 50% mice treated with PGN and WR2721
unitedly could live more than 30 days, while the mice treated with PGN and WR2721 alone died in 9 days
after WBI, and the mice untreated could live less than 5 days after WBI (p<0.01). Conclusions: WBI at a
single dose of 15Gy X-rays would induce GI syndrome, which manifested by less stool formation and lower
body weight with the time post irradiation. At the 5th day after 15Gy WBI, all mice were died. The intestine
cells’ death couldn’t be classified into one kind of death but belonged to “mixed death”. The treatment
effect of PGN and WR2721 unitedly on the WBI mice is better than PGN or WR2721 alone.
(PS3-53) The mechanism and treatment for radiation-induced skin injury: intensification of
antioxidant capability. Shuyu Zhang, Soochow University, Suzhou, China
Ionizing radiation is used extensively to treat many different types of cancer and contributes to
40% of curative cancer treatments. However, radiotherapy may significantly injure the skin and
profoundly impair its function. Radiation-induced skin injury is a serious concern that may limit the
duration and the delivered dose of radiation. However, the molecular mechanism underlying the
pathogenesis of radiation-induced skin injury is largely unknown. Using miRNA microarray, we found that
many miRNAs were significantly dysregulated in irradiated skin tissues, including miR-223, miR-21 and
miR-34a.Using 2-DE and MS, we identified 24 proteins in rat skin tissues irradiated with 45 Gy of electron
beam. These identified differentially expressed proteins included mitochondrial aspartate
217 | P a g e
