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.
Highlights
As a natural focal disease, diabetes is accompanied by an obvious inflammatory response, which plays a crucial role in microvascular complications such as diabetic nephropathy, which has been verified in previous laboratory studies (Lovshin et al, 2017)
The serum tumor necrosis factor-α (TNF-α) levels of kk rat in the thalidomide group and the model control group were both at a higher level before treatment, but there was no significant difference between the groups (P>0.05)
Serum TNF-α, interleukin-1β rat (IL-1β), interleukin -6 (IL-6) and interleukin -18 (IL-18) levels of kk-Ay rats in the thalidomide group decreased significantly after treatment, with statistically significant differences compared with the model control group, suggesting that the use of thalidomide will improve renal inflammatory symptoms effectively in kk-Ay rats
Summary
The existing studies suggest that the pathological mechanism of diabetic nephropathy is related to abnormal glucose metabolism pathway, changes in kidney hemodynamics, cytokines, inflammatory responses and genetic susceptibility factors and etc, and more and more scholars agree on the inflammatory response theory (Zhang et al, 2018; Dionísio et al, 2020a, b; Grom et al, 2020; Wu et al, 2020). As a natural focal disease, diabetes is accompanied by an obvious inflammatory response, which plays a crucial role in microvascular complications such as diabetic nephropathy, which has been verified in previous laboratory studies (Lovshin et al, 2017). 30 kk-Ay rat models were used as experimental animals to further explore the clinical value of thalidomide in improving the damage on kidney tubules epithelial cell through TNF-α mediated inflammatory pathways
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