Abstract
BackgroundRadiation-induced skin injury is a common complication of radiotherapy. The RHIZOMA COPTIDIS and COPTIS CHINENSIS aqueous extract (RCE) can ameliorate radiation-induced skin injury in our clinical observation. But, the protective mechanism of RHIZOMA COPTIDIS and COPTIS CHINENSIS in radiation-induced skin injury remains unclear.MethodsIn this experiment, we developed a radiation-induced skin injury rat model to study the mechanism. The animals were randomly divided into control group, treatment group, radiation group, and treatment and radiation group. 5 rats in each group were separately executed on 2 d and 49 d post-radiation. The semi-quantitative skin injury score was used to measure skin reactions by unblinded observers, and hematoxylin and eosin staining was used to evaluate the damage areas by irradiation. The MDA content, SOD activity of skin and serum were measured to detect the oxidative stress.ResultsAcute skin reactions were caused by a single dose of 45 Gy of β-ray irradiation, and the skin injury could be found in all rats receiving irradiation based on the observation of HE staining of skin at different time-points, while RCE could significantly ameliorate those changes. The MDA content in serum and skin of control rats was 4.13 ± 0.12 mmol/ml and 4.95 ± 0.35 mmol/mgprot on 2 d post-radiation. The rats receiving radiation showed an increased content of MDA (5.54 ± 0.21 mmol/ml and 7.10 ± 0.32 mmol/mgprot), while it was 4.57 ± 0.21 mmol/ml and 5.95 ± 0.24 mmol/mgprot after treated with RCE (p < 0.05). Similar changes of the MDA content could be seen on 49 d post-radiation. However, the SOD activity of rats receiving radiation decreased compared with control group on both time-points, which was inhibited by RCE (p < 0.05). Meanwhile, no valuable changes could be found between control group and treatment group on 2 d and 49 d.ConclusionsOur study provides evidences for the radioprotective role of RCE against radiation-induced skin damage in rats by modulating oxidative stress in skin, which may be a useful therapy for radiation-induced skin injury.
Highlights
Radiation-induced skin injury is a common complication of radiotherapy
A 1.0 cm tissue equivalent bolus was used to bring the maximal dose to the skin surface. 5 rats of each group were separately executed on 2 d and 49 d post-radiation and the skin and blood samples were harvested for the assays of malondialdehyde (MDA), superoxide dismutase (SOD) according to the procedures described below
The order of tissue damages caused by irradiation was as follows: radiation group (R group) (4.8 ± 0.45) > R + treatment group (T group) (3.2 ± 0.45) > T group = control group (C group) (0)
Summary
Radiation-induced skin injury is a common complication of radiotherapy. The protective mechanism of RHIZOMA COPTIDIS and COPTIS CHINENSIS in radiation-induced skin injury remains unclear. The effect of ionization caused by radiation can kill the tumor cell directly or indirectly by generating reactive oxygen species (ROS), free radicals (FR) to cure the disease. We endeavor to maximize anti-cancer effects and minimize skin toxicity, radiation-induced skin injury is the most common complication of radiotherapy, with inflammatory damage caused by radiation on the skin, which may lead to treatment interruptions. Ionizing radiation is known to induce oxidative stress through the generation of ROS and FR, resulting in the imbalance of the pro-oxidant and antioxidant in the cells, which can break the defense system [10]. MDA and SOD are two important compounds in charge of the antioxidant system balance
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