Lime peels are mainly obtained from the byproducts of the juice manufacturing industry, which we obtained and used to extract essential oil (2.3%) in order to examine the antioxidant and hypolipidaemic effects. We identified 60 volatile compounds of lime essential oil (LEO) with GC/MS, of which the predominant constituents were limonene, γ-terpinene, and β-pinene. Lime essential oil was measured according to the DPPH assay and ABTS assay, with IC₅₀ values of 2.36 mg/mL and 0.26 mg/mL, respectively. This study also explored the protective effects of LEO against lipid-induced hyperlipidemia in a rat model. Two groups of rats received oral LEO in doses of 0.74 g/100 g and 2.23 g/100 g with their diets. Eight weeks later, we found that the administration of LEO improved the serum total cholesterol, triglyceride, low-density lipoprotein cholesterol, alanine aminotransferase, and aspartate transaminase levels in the hyperlipidemic rats (p < 0.05). Simultaneously, the LEO improved the health of the rats in terms of obesity, atherogenic index, and fatty liver.

Previous studies have revealed the anti-inflammatory and neuroprotective properties of Hericium erinaceus extracts, including the fact that the active ingredient erinacine C (EC) can induce the synthesis of nerve growth factor. However, there is limited research on the use and mechanisms of action of EC in treating neuroinflammation. Hence, in this study, the inflammatory responses of human BV2 microglial cells induced by LPS were used to establish a model to assess the anti-neuroinflammatory efficacy of EC and to clarify its possible mechanisms of action. The results showed that EC was able to reduce the levels of nitric oxide (NO), interleukin-6 (IL-6), tumor necrosis factor (TNF)-α, and inducible nitric oxide synthase (iNOS) proteins produced by LPS-induced BV2 cells, in addition to inhibiting the expression of NF-κB and phosphorylation of IκBα (p-IκBα) proteins. Moreover, EC was found to inhibit the Kelch-like ECH-associated protein 1 (Keap1) protein, and to enhance the nuclear transcription factor erythroid 2-related factor (Nrf2) and the expression of the heme oxygenase-1 (HO-1) protein. Taken together, these data suggest that the mechanism of action of EC involves the inhibition of IκB, p-IκBα, and iNOS expressions and the activation of the Nrf2/HO-1 pathway.