Clinical value of thalidomide on kk-rat model through TNF-a mediated inflammation approach

• Autor(a) principal: HUANG,Min
• Data de Publicação: 2022
• Outros Autores: DUAN,Jie, YU,Bin, ZHENG,Si-lin, CHEN,Qi, LIN,Fei, ZENG,Nan, LING,Bao-dong
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Food Science and Technology (Campinas)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000100530
• topic: thalidomide; tucorrelation mor necrosis factor –α; interleukin-1β; kidney tubules epithelial cell

Abstract To observe the influence of thalidomide on tumor necrosis factor-a (TNF-α) of spontaneous type-2 diabetes rat (kk-Ay rat) model, and to explore the clinical value of TNF-a mediated inflammation approach to improve the injury on epithelial cell of kidney tubules. There are 30 kk-Ay rates being chosen to establish the Diabetic Nephropathy model and divided into thalidomide group and the model control group, 15 pieces for each group respectively. The levels of TNF-α, IL-1β, interleukin -6 (IL-6) and interleukin -18 (IL-18) of kk-Ay in the thalidomide group and the model control group were both at a higher level before treatment, but the difference was not statistically significant (P >0.05); The levels of TNF-α, IL-1β, interleukin -6 (IL-6) and interleukin -18 (IL-18) in kk-Ay rats 8/10/12 weeks after the treatment in the thalidomide group were significantly decreased, with statistically significant differences compared with the model control group (P < 0.05). The histopathological changes of kidney tubules epithelial cell injury on rats were observed through dissection. Thalidomide will effectively lower TNF-α and IL-1β expression levels in kk-Ay rat models, reduce inflammatory response, and thus improve damage on kidney tubules epithelial cell, which is worthy of further exploration and application.