Background Acute cadmium (Cd) exposure can cause damage to multiple tissues, with the kidney being the primary target organ. The development of Cd-induced acute kidney injury involves complex mechanisms, in which autophagy and oxidative stress play crucial roles.

Objective To investigate the effect of 10-hydroxy-2-decenoic acid (10-HDA) on kidney injury in mice exposed to cadmium, and provide experimental basis for studying the pathogenesis and prevention of Cd poisoning.

Methods Thirty-five male C57BL/6 mice were divided into 7 groups (each of 5 mice): control group (normal saline, intraperitoneal injection), CdCl₂ group (4 mg·kg⁻¹, intraperitoneal injection), intervention groups ( 4 mg·kg⁻¹ CdCl₂, intraperitoneal Injection + 50, 100, 150, or 200 mg·kg⁻¹ 10-HDA, oral gavage), and 10-HDA group (150 mg·kg⁻¹, oral gavage). All treatments were given for 14 d. Twenty-four hours after the last infection, physiological indicators blood urea nitrogen (BUN), creatinine (CRE), malondialdehyde (MDA), and superoxide dismutase (SOD), histopathological indicators, autophagy-related proteins (Atg7, Atg5, Beclin-1, and LC3), and mitochondrial autophagy-related proteins (PINK1 and Parkin) were detected to examine the effect of 10-HDA on kidney injury caused by CdCl₂.

Results Compared with the control group, the body weight of mice in the CdCl₂ group was significantly reduced (P<0.01); compared with the CdCl₂ group, the body weight of mice after intervention with different concentrations of 10-HDA was significantly increased (P<0.01). CdCl₂ significantly increased BUN and CRE in the serum samples compared with the control group (P<0.01), which was significantly reduced to varying degrees after 100, 150, and 200 mg·kg⁻¹ 10-HDA intervention (P<0.01). MDA significantly increased and SOD significantly decreased in the renal cortex following CdCl₂ administration compared with the control group (P<0.01), which was resolved following 10-HDA administration at different concentrations (P<0.01). In histopathological studies, 10-HDA restored injured kidney tissues induced by CdCl₂. The expression levels of autophagy proteins Atg7 and LC3-II/I were significantly increased (P<0.05), and the expression level of Beclin-1 was significantly decreased (P<0.05) in the CdCl₂ group compared with the control group. The expression levels of Atg7 were reduced to varying degrees after treatment with designed concentrations of 10-HDA, the expression levels of LC3-II/I were also reduced in the 50, 150, and 200 mg·kg⁻¹ 10-HDA intervention groups, and the expression levels of Beclin-1 were increased in the 50, 100, and 150 mg·kg⁻¹ 10-HDA intervention groups (P<0.05). The expression levels of PINK1 and Parkin in the CdCl₂ group and the 50 mg·kg⁻¹ 10-HDA intervention group were lower than those in the control group (P<0.01). Compared with the CdCl₂ group, the expression levels of PINK1 increased to varying degrees after 100, 150, and 200 mg·kg⁻¹ 10-HDA intervention, and the expression levels of Parkin increased in all 10-HDA intervention groups (P<0.01).

Conclusion The intervention using 10-HDA can lessen acute kidney injury caused by CdCl₂, reduce the expression of autophagy-related proteins, and increase the expression of mitochondrial autophagy-related proteins.