Chronic Exposure to Various Propolis Extracts from North Sumatra Does Not Trigger Hepatic Inflammation and Autophagy Gene Expression in Wistar Rats
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Abstract
The liver has key roles in metabolism, detoxification, and immunity, making it prone to inflammation and autophagy disruption. Natural bioactive compounds, such as stingless bee propolis, have been studied for their potential protective effects on various organs, including the liver. The purpose of this work was to analyze the phytochemical compounds of different propolis types and their effects on inflammation (IL-6 and TNF-α) and autophagy (LC3 and p62) gene expression in the liver. Propolis was obtained from different regions of North Sumatra, Indonesia (Karo Regency, Langkat Regency, and Tapanuli Tengah Regency), produced by two stingless bee species: Geniotrigona thoracica (Propolis A, B, C) and Tetrigona apicalis (Propolis D). Twenty-five Wistar rats (12 weeks old) were divided into five groups: a control group and four treatment groups receiving Propolis A, B, C, and D, each at an approximate dose of 100 mg/kg/day. Propolis was administered daily via drinking water for six consecutive months. Phytochemical screenings were conducted, and inflammation and autophagy gene expressions were evaluated using real-time polymerase chain reaction (PCR). Different phytochemical compounds were found in the four different propolis types, with Propolis B showing the most abundant phenolics, tannins, flavonoids, triterpenoids, and saponins. No significant difference in IL-6 and TNF-α gene expression was found between groups. The study highlights that chronic exposure to various propolis types does not induce hepatic inflammation or autophagy-related gene expression in healthy Wistar rats, while also suggesting that bee species and regional origin may influence their phytochemical composition and bioactivity.
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