High fat diet (HFD) is a risk factor for various diseases in humans and animals. Metabolic disease‑induced
brain injury is becoming an increasingly popular research topic.
Carnosic acid (CA) is a phenolic
diterpene synthesized by plants belonging to the Lamiaceae family, which exhibits multiple
biological activities. In the present study, a mouse model of HFD‑induced
metabolic syndrome was generated. The
body weight, liver weight, daily food intake, daily caloric intake, serum TG, serum TC, serum
insulin and serum
glucose of animals treated with CA were recorded. Additionally, the gene and
protein expression levels of inflammatory
cytokines, NF‑κB signaling componnts, and caspase‑3 were evaluated in the various CA treatment groups via immunohistochemical analysis, western blotting, reverse transcription‑quantitative PCR. CA treatment significantly decreased HFD‑induced
metabolic syndrome by decreasing the serum levels of
triglycerides, total
cholesterol,
insulin and
glucose. Furthermore, CA served a protective role against
brain injury by inhibiting the inflammatory response. CA significantly decreased the
protein expression levels of various pro‑inflammatory
cytokines in serum and brain tissues, including
interleukin (IL)‑1β, IL‑6 and
tumor necrosis factor‑α, regulated by the NF‑κB signaling pathway. In addition, CA was revealed to promote the expression levels of anti‑apoptotic Bcl‑2, and to decrease the expression levels of pro‑apoptotic Bax and matrix
metallopeptidase 9. The present results suggested that CA was able to alleviate
brain injury by modulating the inflammatory response and the apoptotic pathway. Administration of CA may represent a novel therapeutic strategy to treat metabolic disease‑induced
brain injury in the future.