The occurrence and development of radiation-induced lung injury after interstitial brachytherapy and stereotactic radiotherapy in SD rats

Abstract

Background To compare the severity of radiation-induced lung injury (RILI) after the right lung of SD rats received interstitial brachytherapy and stereotactic radiotherapy (SBRT). Methods RILI rat model was established using interstitial brachytherapy and SBRT methods, respectively. CT scan was performed to analyze the lung volume and the CT value difference between the left and right lungs in rats. Then the lung tissues were analyzed through H&E staining, peripheral blood was extracted to detect the expression levels of serum inflammatory cytokines, pro-fibrotic cytokines, and fibrotic-inhibiting cytokines by ELISA. Results The difference between right and left lung CT values was significantly elevated in the SBRT group when compared with the control group and the interstitial brachytherapy group (P < 0.05). The IFN-γ expression in the interstitial brachytherapy group was significantly different from that in the SBRT group at week 1, 4, 8 and 16. Besides, the expressions of IL-2, IL-6 and IL-10 in SBRT group were significantly higher than that of interstitial brachytherapy group (P < 0.05). The TGF-β expression in interstitial brachytherapy group reached its peak with the increase of time from week 1 to week 16, and it was significantly lower than SBRT group (P < 0.05). The mortality rate in the SBRT group was 16.7%, which was significantly higher than that in the interstitial brachytherapy group. Conclusion The treatment method of interstitial brachytherapy is considered as an effective and safe tool by reducing the side effects of radiotherapy and increasing the radiation dose of radiotherapy.

Flavone attenuates nicotine-induced lung injury in rats exposed to gamma radiation via modulating PI3K/Nrf2 and FoxO1/NLRP3 inflammasome

“…Collectively, the excessive ROS resulting from exposure to both toxin nicotine and γ-IR act synergistically as inflammatory signaling molecules in the lung to stimulate alveolar macrophages and neutrophils 42 , 43 as well as many pro-inflammatory transcription factors (NF-κB due to the proteasomal degradation of IκBα 35 and protein (NLRP3) leading to upregulation of the pro-inflammatory cytokine TNF-α coupled with infiltration of many inflammatory cells and edema which ultimately induced lung tissue damage and injury. 9 , 44 Accordingly, our results are in line with previous data indicating that nicotine activated NF-κB which aggravates the release of the pro-inflammatory cytokines TNF-α in lung tissues.…”