Abstract: Objective To explore the correlation between histone methyltransferase 2 (SMYD2) and cisplatin-induced inflammatory response in chronic kidney disease (CKD), and provide a new direction for the clinical prevention and treatment of cisplatin-induced CKD. Methods Sixteen mice were divided into the control group and the cisplatin group according to the random number table method, with 8 mice in each group. Mice in the cisplatin group were injected intraperitoneally with 10 mg/kg cisplatin, and in the control group, the same volume of cisplatin solvent was injected once a week for 3 consecutive weeks. At the fourth week, the mice were sacrificed and serum and kidney tissue were collected. Automatic biochemical analyzer was used to detect blood urea nitrogen (BUN) and blood creatinine (Scr). HE and Masson staining was used to observe renal histopathological changes. Western blot assay was used to detect renal tissue SMYD2, α- smooth muscle actin (α-SMA), waveform protein (Vimentin), E-cadherin, Fibronectin, Collagen-Ⅲ, signal transducer and activator of transcription 3 (STAT3), p-STAT3, tumor necrosis factor- α (TNF- α) and interleukin-6 (IL-6). Results Compared with the control group, the BUN and Scr levels were significantly increased in the cisplatin group (P＜0.05). Some glomeruli in kidney showed mesangial cell proliferation, granular degeneration and vacuole-like changes in renal tubules. The proliferation of interstitial fibers was obvious. The expression levels of SMYD2, α -SMA, Vimentin, Fibronectin, Collagen-Ⅲ, STAT3, p-STAT3, TNF-α and IL-6 protein increased, and the protein expression of E-cadherin decreased (P＜0.05). There was a negative correlation between SMYD2 and the expression of E-cadherin. There was a positive correlation between SMYD2 and expression levels of α-SMA, Vimentin, Fibronectin, Collagen-Ⅲ, STAT3, p-STAT3, TNF- α, and IL-6 (P＜0.05). Conclusion SMYD2 is upregulated in kidney of cisplatin-induced CKD mice. It is speculated that SMYD2 may be involved in the inflammation together with the STAT3 signaling pathway and participate in the occurrence development of cisplatin-induced CKD.

Key words: chronic disease, kidney diseases, cisplatin, protein methyltransferases, STAT3 transcription factor, histone methyltransferase 2, renal fibrosis, inflammatory response