Bisphenol A is an environmental pollutant that induces oxidative stress in the kidney. Phytochemicals such as
cinnamic acid have been demonstrated to possess antioxidative properties that could mitigate against oxidative stress.
The current study investigates underlying pathways that may help elucidate the protective role of cinnamic acid (CA)
against bisphenol A (BPA)-induced nephrotoxicity. Rats were divided randomly into five groups. Group 1 was the
control. Group 2 took BPA only. Group 3 was given BPA combined with CA (50 mg/kg), while group 4 had BPA
and cinnamic acid (100 mg/kg). Group 5 received cinnamic acid only (100 mg/kg). Antioxidant parameters and protein
expression levels were evaluated. Bisphenol A at 100 mg/kg significantly increased urea concentration and lipid
peroxidation. Glutathione (GSH) level decreased, and superoxide dismutase (SOD), catalase, and glutathione-S-
transferase (GST) presented lower activities than in the control (P>0.05). Cinnamic acid improved renal function by
significantly reducing urea levels. Oxidative stress was reduced, as evidenced by lower malondialdehyde and higher
antioxidant marker levels (GSH, SOD, catalase, and GST) compared with the BPA-administered group. qRT-PCR
results showed a decline in Nrf2 expression in BPA-treated rats compared with the control (P<0.05). However, this
decline was reversed upon CA treatment. Cinnamic acid at 100 mg/kg to rats treated with bisphenol A preserved the
structural integrity of the kidney. The data obtained suggests that cinnamic acid’s protective effect against BPA-
induced nephrotoxicity may be driven by its ability to decrease oxidative stress and reduce inflammation through
regulation of Nrf2 signaling pathway.