#Exposure x activation code skin
#Exposure x activation code plus
#Exposure x activation code free

Therefore, preventing the production of ROS or increasing the content of endogenous antioxidants is of great significance for the prevention and treatment of RISI.

On the other hand, ROS contribute to the activation of DNA damage and senescence pathways in irradiated cells. In addition, ROS production is the most important trigger for the formation and activation of NLRP3 inflammasome.

#Exposure x activation code free

The overproduction of free radicals and reactive oxygen species (ROS) induced by radiation may give rise to oxidative stress reaction, damage the basal cells of the skin, and prevent the basal cells from division, proliferation, differentiation, and keratinization to induced RISI. Studies have shown that the oxidation/reduction (redox) system played a key role in acute radiation-induced injury and regulated a number of effects, such as bystander effects, out-of-field effects, inflammation, and fibrosis. Therefore, modulation of targets associated with NLRP3 inflammasomes may serve as a novel therapeutic strategy for RISI. In addition, previous reports have shown that inflammation can inhibit DNA damage repair responses. Studies suggested that expression upregulation of NLRP3 inflammasome played an important role in radiation damage, including RISI. Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome can activate caspase-1, leading to the maturation and release of inflammatory cytokines, including IL-1ОІ and IL-18. Inflammasome-activation-mediated inflammation is an important part of the inflammatory response. In addition, studies have shown that oxidative stress and inflammatory response may be related to the pathogenesis of RISI. IR can cause DNA strand breaks and a large amount of DNA damage in cells, which can lead to radiation damage. RISI can affect the dose and tolerance of RT in cancer patients, leading to decreased quality of life and poor tumor control.

#Exposure x activation code skin

It has been reported that about 80% of patients with head and neck cancer during RT can present dry or wet dermatitis, mucosal congestion, erosion, ulcers, and other skin mucosal reactions after RT. Radiation-induced skin injury (RISI) is one of the major complications. Common complications include fatigue, hematological toxicity, skin and mucous membrane damage, and damage to other exposed sites. While killing tumors, radiation can also bring both short-term and long-term side effects to healthy tissue. Radiotherapy (RT) is currently the main treatment for various cancers. SFN may be able to suppress the oxidative stress by upregulating the expression and function of Nrf2, and subsequently inhibiting the activation of NLRP3 inflammasome and DNA damage, so as to prevent and alleviate the RISI. In addition, the expressions of Nrf2 and its regulated antioxidant enzymes, including CAT and HO-1, were higher in the skin tissues of SFN and IR/SFN groups, but lower in the control and IR groups ( p < 0.05). However, the above pathological changes declined sharply after SFN treatment ( p < 0.05). Western blotting and ELISA results showed that the inflammasome of NLRP3, caspase-1, and IL-1ОІ, as well as oxidative stress damage indicators ROS, 4-HNE, and 3-NT, in the skin tissues of mice in the IR group were significantly higher than those in the control group ( p < 0.05). The H&E staining showed the hyperplasia of fibrous tissue in the mouse dermis and hypodermis of the IR group.

Then, the oxidative stress and inflammatory response indexes in mouse skin tissues, as well as the expression of Nrf2 and its downstream antioxidant genes, were evaluated by ELISA, real-time PCR, and Western blotting. At eight weeks after irradiation, the morphological changes of mouse skin tissues were detected by H&E staining.

#Exposure x activation code plus

Thirty-two C57/BL6 mice were randomly divided into control group (CON), SFN group, irradiation (IR) group, and IR plus SFN (IR/SFN) group. The RISI model was established by the irradiation of the left thigh under intravenous anesthesia. In addition, we will discuss the mechanism of SFNвЂ™s protection on RISI. This article mainly observed the protective effect of sulforaphane (SFN) on radiation-induced skin injury (RISI).