Lactobacillus plantarum LP33 attenuates Pb-induced hepatic injury in rats by reducing oxidative stress and inflammation and promoting Pb excretion

Lead (Pb) is one of the most common heavy metals and is harmful to human health. The liver is considered as a major target organ for Pb poisoning. Although probiotics have been shown to alleviate liver injury, the protective effect of Lactobacillus plantarum LP33 (LP33) against Pb-induced hepatotoxicity remains unclear. In order to explore the hepatoprotective effect of LP33, LP33 was administered to Pb-intoxicated Sprague-Dawley rats once daily by oral gavage for 8 weeks. The present results showed that LP33 supplementation alleviated liver injury, and inhibited oxidative stress and inflammation in Pb-exposed rats. Treatment with LP33 also promoted the phosphorylation of adenosine monophosphate-activated protein kinase and protein kinase B, activated nuclear factor erythroid 2-related factor 2 signaling and inhibited the activation of nuclear factor-KB signaling in liver tissues of rats exposed to Pb. Additionally, LP33 exhibited adequate Pb-binding capacity and satisfactory survival under simulated gastrointestinal conditions in vitro, and promoted Pb excretion via enterohepatic circulation of bile acids. This study demonstrated that LP33 reduced Pb-induced oxidative stress and inflammation and promoted Pb excretion, thereby attenuating the Pb-induced hepatic injury. Our findings suggest that LP33 supplementation may be a potential strategy for the treatment of Pb-induced hepatic toxicity.