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PubMed1977

[Experiments on the biosynthesis of UDP-Glucuronyltransferase and UDP-Glucosyltransferase under the influence of eucalyptol (author's transl)].

To elucidate the reaction mechanism of the increased elimination rate of bilirubin in the blood of newborns under the influence of Eucalyptol, we performed a study on young mice. The following results were obtained: UDPGA-T activity is increased 33%, if measured with 4-MU as substrate after a single injection (i.p.) of Eucalyptol (0.3 mg/g body weight), with bilirubin as substrate the increase is 112%. UDPG-T activity increases 29%. The enhancement of enzyme activities can be inhibited by Actinomycin D (1 MUg/g body weight) 30% (bilirubin), 48% (4-MU) respectively in the case of UDPGA-T. Under cycloheximide (2 mug/g body weight) the increase of the activity of UDPGA-T is suppressed by 59% (bilirubin) or 99% (4-MU) as compared to the corresponding controls. No significant difference in the activity of UDPG-T by actinomycin or cycloheximide can be observed between the controls and the Eucalyptol-treated group. We conclude that the increase of enzyme activity of UDPGA-T is mainly due to enzyme induction, while in the case of UDPG-T activation of enzyme molecules might be the underlying mechanism. The effect of Eucalyptol on the bilirubin level in the blood of newborns is comparable to the effect of phenobarbital.

Animals↗
PubMed2026

Eucalyptol mitigates isoproterenol-induced myocardial injury in rats via activation of p38 MAPK/JNK signaling, suppression of ER stress, and modulation of apoptotic pathway.

BACKGROUND: Myocardial injury (MI), a subset of cardiovascular diseases, remains a leading cause of deaths globally, driven by pathological inflammation, oxidative stress, and apoptosis. Despite advances in interventional cardiology, high relapse rates and therapeutic limitations underscore the urgent need for novel pharmacological agents. Phytochemicals, with their multi-target approach and favorable safety profiles, offer promising alternatives for mitigating ischemic injury. METHODS: The cardioprotective effects of 1,8-cineole, a monoterpene derived from Eucalyptus species, was investigated in a rat model of isoproterenol-induced myocardial injury. Serum levels of cardiac enzymes (creatine kinase (CK), lactate dehydrogenase (LDH)) and pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) were quantified. Preliminary histopathological analysis was performed to assess the extent of myocardial damage. Key molecular mechanisms were evaluated via western blotting and immunohistochemistry, examining pathways related to inflammation (NF-κB), apoptosis (Bcl-2/Bax, caspase-3), endoplasmic reticulum (ER) stress (GRP78, CHOP, PERK-eIF2α), and antioxidant defense (GSH, SOD, CAT). RESULTS: Our results demonstrate that 1,8-cineole significantly reduced the levels of serum cardiac enzymes (CK-MB, LDH), and histopathological damage. Mechanistically, 1,8-cineole also suppressed pro-inflammatory cytokine release (TNF-α, IL-6, and IL-1β) via inhibition of the NF-κB pathway. Furthermore, it attenuated cardiomyocyte apoptosis by modulating Bcl-2/Bax expression and inhibiting caspase-3 activation. Additionally, 1,8-cineole alleviated ER stress by downregulating GRP78, CHOP, and PERK-eIF2α signaling. Importantly, we identified enhanced Nrf2 nuclear translocation and subsequent upregulation of antioxidant enzymes (GSH, SOD, CAT) as key contributors to its cytoprotective effects. CONCLUSIONS: 1,8-Cineole exhibits potent cardio-protection in experimental myocardial injury by targetinginflammation, apoptosis, ER stress, and oxidative stress through modulation of p38 MAPK/JNK, suppression of inflammatory markers (TNF-α, IL-6, IL-1β) and apoptotic markers (Bax, p53). Its natural origin, bioavailability, and multi-mechanistic effectiveness make it a promising candidate for translational development as an adjunct therapy for myocardial injury.

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