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Abstract Title:

Carnosic acid alleviates brain injury through NF‑κB‑regulated inflammation and Caspase‑3‑associated apoptosis in high fat‑induced mouse models.

Abstract Source:

Mol Med Rep. 2019 Jul ;20(1):495-504. Epub 2019 May 27. PMID: 31180544

Abstract Author(s):

Yong Liu, Yan Zhang, Ming Hu, Yu-Hu Li, Xing-Hua Cao

Article Affiliation:

Yong Liu

Abstract:

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.

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