ABSTRACT
Objective To explore the inhibitory effect of captopril on acute radiation-induced lung injury in rats and the possible mechanism. Methods Sixty-four female Wistar rats were randomly divided into control group, irradiation group, irradiation+low-dose captopril group, and irradiation+high-dose captopril group. A single dose of 20 Gy was given to the right lung of all rats except those in the control group to establish a rat model of acute radiation-induced lung injury. These rats were sacrificed at 1, 2, 4, and 8 weeks. HE staining was used to observe the pathological changes in lung tissue;RT-PCR and Western blot were used to measure the mRNA and protein expression of CCL-2 in lung tissue;immunohistochemical assay was used to determine the number of monocytes ( CD68 ) in lung tissue. A one-way analysis of variance was performed. Results Captopril significantly reduced lung inflammation in rats with acute radiation-induced lung injury (P<005), inhibited the accumulation of monocytes (CD68) in lung tissue (P<005), and decreased the content of CCL-2 in lung tissue ( P<005 ) . Conclusions For rats with acute radiation-induced lung injury, captopril can reduce the expression of CCL-2 to inhibit the accumulation of monocytes in lung tissue and thus attenuate lung inflammation.
ABSTRACT
Objective To explore the inhibitory effect of captopril on acute radiation-induced lung injury in rats and the possible mechanism. Methods Sixty-four female Wistar rats were randomly divided into control group, irradiation group, irradiation+low-dose captopril group, and irradiation+high-dose captopril group. A single dose of 20 Gy was given to the right lung of all rats except those in the control group to establish a rat model of acute radiation-induced lung injury. These rats were sacrificed at 1, 2, 4, and 8 weeks. HE staining was used to observe the pathological changes in lung tissue;RT-PCR and Western blot were used to measure the mRNA and protein expression of CCL-2 in lung tissue;immunohistochemical assay was used to determine the number of monocytes ( CD68 ) in lung tissue. A one-way analysis of variance was performed. Results Captopril significantly reduced lung inflammation in rats with acute radiation-induced lung injury (P<005), inhibited the accumulation of monocytes (CD68) in lung tissue (P<005), and decreased the content of CCL-2 in lung tissue ( P<005 ) . Conclusions For rats with acute radiation-induced lung injury, captopril can reduce the expression of CCL-2 to inhibit the accumulation of monocytes in lung tissue and thus attenuate lung inflammation.
ABSTRACT
BACKGROUND: The radiation-induced lung injury is a common complication from radiotherapy in lung cancer. CpG ODN is TLR9 activator with potential immune modulatory effects and sensitization of radiotherapy in lung cancer. This study aimed to examine the effect of CpG ODN on acute radiation-induced lung injury in mice. METHODS AND RESULTS: The mouse model of radiation-induced lung injury was established by a single dose of 20 Gy X-rays exposure to the left lung. The results showed that the pneumonia score was lower in RT+CpG group than in RT group on 15th and 30th days. Compared with RT group, CpG ODN reduced the serum concentrations of MDA (P < 0.05) and increased the serum concentrations of SOD, GSH (P < 0.05). The serum concentration of TNF-α in RT+CpG group was lower on 15th and 30th days post-irradiation (P < 0.05). CONCLUSION: The study demonstrated that CpG ODN has preventive effects of acute radiation-induced lung injury in mice. Lung inflammatory reaction and oxidative stress are promoted in the initiation of radiation-induced pneumonia. CpG ODN may reduce the injury of reactive oxygen species and adjust the serum TNF-α concentration in the mice after irradiation, which reduces the generation of the inflammatory cytokines.
Subject(s)
Animals , Mice , Oligodeoxyribonucleotides/pharmacology , Radiation Injuries, Experimental/prevention & control , Acute Lung Injury/prevention & control , Pneumonia/etiology , Pneumonia/pathology , Pneumonia/prevention & control , Radiation Injuries, Experimental/blood , Superoxide Dismutase/blood , Time Factors , Severity of Illness Index , Enzyme-Linked Immunosorbent Assay , Reproducibility of Results , Tumor Necrosis Factor-alpha/blood , Disease Models, Animal , Acute Lung Injury/etiology , Acute Lung Injury/pathology , Acute Lung Injury/blood , Glutathione/blood , Malondialdehyde/bloodABSTRACT
Objective To investigate the radioprotective function of lianhuaqingwen (LHQW) in rat acute radiation-induced lung injury.Methods Totally 36 female Wistar rats were randomized into 3 groups as administered group (treated by LHQW plus radiation),radiation group irradiated with a single of 20 Gy in 6 MV X-ray by Elekta Synergy VMAT,and blank control group without radiation.Performance status (PS) was estimated during 31 d of LHQW instragastric administration.After rats being sacrificed at 1,14,28 d of LHQW adminstration,the pathomorphological changes were observed in trauma lung tissue,the cell number in BALF (Bronchoalveolar lavage fluid) was counted,the levels of TNF-α and IL-6 in serum were measured by ELISA,and TNF-α and IL-6 mRNA expressions in lung tissue were assayed by RT-PCR.Results After LHQW treatment,the PS of rat was significantly elevated with less inflammation in morphous,and the cell number in BALF was markedly decreased in compare with radiation alone group.Furthermore,the serum levels of TNF-α and IL-6 were obviously reduced (tTNF-α =7.372,2.891,tIL-6 =6.335,3.257,P ＜ 0.05) and the TNF-α and IL-6 mRNA levels in lung tissue were also decreased (tTNF-αmRNA =3.714,2.144,tIL-6mRNA =3.589,2.883,P＜0.05).Conclusions LHQW plays a protective role against acute radiation-induced lung injury in rats and the down-expressions of TNF-α and IL-6 may be involved.