Advances and Challenges in the Analysis of Boswellic Acids by Separation Methods

Boswellia resin is an exudate from the cut bark of Boswellia trees. The main constituents of pharmacological interest are boswellic acids (pentacyclic triterpenoids), namely α-boswellic acid, β-boswellic acid, 3-O-acetyl-α-boswellic acid, 3-O-acetyl-β-boswellic acid, 11-keto-β-boswellic acid, and 3-O-acetyl-11-keto-β-boswellic acid. Nowadays, dietary supplements with Boswellia serrata extract are used in the treatment of inflammatory joint diseases. Additionally, the constituents of Boswellia resin have shown potential for the treatment of other chronic inflammatory diseases and various types of cancer. Separation methods including ultra/high-performance liquid chromatography, gas chromatography, thin layer chromatography, supercritical fluid chromatography, and capillary electrochromatography coupled with UV or MS detection have been used for the determination of boswellic acids in various matrices (mostly plant material and biological samples). This review aims to provide a comprehensive summary of these separation methods, offering a critical discussion of their strengths and limitations in the analysis of boswellic acids. The knowledge of various separation methods plays a pivotal role in the quality control of herbal dietary supplements and the monitoring of the metabolism and pharmacokinetics of their constituents. The approaches based on metabolomics and network pharmacology represent new ways of fingerprinting secondary metabolites in Boswellia resin increasing the comprehensiveness of the output of these methods resulting in safer dietary supplements.</p

Hemi-body UPDRS-III subscores in the sON condition after overnight withdrawal of dopaminergic therapy in relation to the mediolateral position of the contralateral active contact.

<p>After initiation of STN-DBS, the hemi-body side with the lowest motor score (best motor condition) had the contralateral contacts located more laterally from the wall of the third ventricle (r = −0.42, p<0.01). Dotted lines denote the 95% confidence interval of the regression line.</p

Weight gain in 20 patients with Parkinson's disease in relation to the mediolateral position of the active contact with bilateral STN-DBS (r = −0.55, p<0.01).

<p>Only one active contact (more medial contact from both hemispheres) was used in each patient. The x-coordinate represents the distance of the active contact from the wall of the third ventricle. Each millimeter in the medial direction was associated on average with a 1.6-kg increase in body weight. Dotted lines denote the 95% confidence interval of the regression line.</p

Bilateral STN-DBS active contact positions of 20 patients with Parkinson's disease plotted in the coronal plane with respect to weight gain.

<p>Patients (N = 11) with at least one active contact (a) placed within 9.3-mm of the wall of the third ventricle gained significantly more weight than patients (N = 9) with both contacts (b) located more laterally (p<0.001).</p

Mean changes in weight after implantation in 20 patients with Parkinson's disease.

<p>Body weight gradually increased during the study period. Weight gain represents the difference in weight (±SD) compared to the preoperative state.</p

Intravenous rutin in rat exacerbates isoprenaline-induced cardiotoxicity likely due to intracellular oxidative stress

<p><b>Objectives</b>: Rutin, quercetin-3-<i>O</i>-rutinoside, a natural flavonol glycoside, has shown various <i>in vitro</i> benefits with potential use treating human diseases, especially cardiovascular system disorders. Antioxidant properties are assumed to underlie the majority of these benefits. Yet rutin pro-oxidant properties have been reported as well. Our research group has recently shown aggravating effects on isoprenaline (ISO)-induced cardiotoxicity in Wistar:Han rats after 24 hours.</p> <p><b>Methods</b>: This study was designed to examine in more detail the reasons for the negative effects of rutin (11.5 and 46 mg/kg, i.v.) after administration of ISO (100 mg/kg, s.c.) in rats within 2 hours of continuous experiment and in the H9c2 cardiomyoblast-derived cell line.</p> <p><b>Results</b>: Like our previous findings, rutin did not (11.5 or 46 mg/kg, i.v.) reduce the ISO-induced mortality within 2 hours although the lower dose significantly reduced cardiac troponin T (cTnT) and partly improved the histological findings. In contrast, the higher dose increased the mortality in comparison with solvent (1.26% w/v sodium bicarbonate). This was not caused by any specific haemodynamic disturbances. It appears to be associated with oxidative stress as rutin enhanced intracellular reactive oxygen species formation <i>in vitro</i> and had the tendency to increase it <i>in vivo</i>.</p> <p><b>Conclusions</b>: Rutin, likely due to its pro-oxidative effects, can exacerbate catecholamine cardiotoxicity depending on the dose used.</p