Abstract
Evodiae fructus (EF) has been used in China for thousands of years as an analgesic, antiemetic, anti-inflammatory and antidiarrheal drug. EF is a toxic drug and causes hepatotoxicity in humans. Although recent chronic toxicity studies performed on aqueous extract of EF has revealed that it can produce obvious cumulative hepatotoxicity, the mechanism behind this toxicity is still uncertain. In the present study, we investigated the influence of EF on oxidative stress, mitochondrial permeability transition, adenosine triphosphate (ATP), and cytochrome C release of hepatic mitochondria. Rats were divided into four groups and fed distilled water, 6, 12, 24 g/kg of aqueous extract of EF daily for 15 days. Evodiamine, rutaecarpine and evodine were quantified in the aqueous extract by high performance liquid chromatography with ultraviolet detection (HPLC/UV). The results showed that aqueous extract of EF could significantly (p < 0.05) decrease MnSOD levels to 56.50%, 46.77% and 19.67% of control group, GSH level was decreased to 74.24%, 53.97% and 47.91% of control group and MDA level was increased to 131.55%, 134.34% and 150.81% of control group in the 6, 12 and 24 g/kg groups, respectively; extract also induced mitochondria swelling, vacuolation, MPT pore opening and a significant decrease (p < 0.05) in mitochondrial potential, while ATP levels were significant decreased (p < 0.05) to 65.24%, 38.08% and 34.59% of control group in the 6, 12 and 24 g/kg groups, respectively, resulting in ATP depletion and CytC release, finally trigger cell death signaling, which are the partial hepatotoxicity mechanisms of EF.
Highlights
Evodiae fructus (EF, known in Chinese as Wu Zhu Yu), is the dried, nearly ripe fruit of Evodia rutaecarpa (Juss.) Benth
EF has been used for thousands of years in China, mainly used in prescriptions; its therapeutic efficacy is supported by clinical patients but lacks evidence-based medicine (EBM) proof, which are encouraging for both prescription and individual traditional Chinese medicine (TCM) herbs
We investigated the capability of EF to induce oxidative stress and mitochondrial permeability transition (MPT) by using mitochondria isolated from the liver of rats which were orally administered aqueous extract of EF for 15 days
Summary
Evodiae fructus (EF, known in Chinese as Wu Zhu Yu), is the dried, nearly ripe fruit of Evodia rutaecarpa (Juss.) Benth. Alkaloids are major bioactive ingredients in EF, and many recent studies have focused on the pharmaceutical potential of these alkaloids, such as the major alkaloid evodiamine, which induces apoptosis and G2/M arrest in human colorectal carcinoma cells [3], inhibits the growth of human colon carcinoma cells [4] and hepatoblastoma cell lines [5] Rutaecarpine, another alkaloid in EF, exhibits interesting pharmaceutical activity, such as suppressing atherosclerosis [6], and vasodilation for treatment of cardiovascular disorders [7]. Evodiamine, rutaecarpine and evodine, the major components of EF, were quantified by high performance liquid chromatography with ultraviolet detector (HPLC/UV) analysis of EF
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