Boswellic acids inhibit glioma growth: a new treatment option?

Citation
M. Winking et al., Boswellic acids inhibit glioma growth: a new treatment option?, J NEURO-ONC, 46(2), 2000, pp. 97-103
Citations number
31
Categorie Soggetti
Oncology
Journal title
JOURNAL OF NEURO-ONCOLOGY
ISSN journal
0167594X → ACNP
Volume
46
Issue
2
Year of publication
2000
Pages
97 - 103
Database
ISI
SICI code
0167-594X(2000)46:2<97:BAIGGA>2.0.ZU;2-E
Abstract
Conventional malignant glioma therapy (surgery, radiation therapy and chemo therapy) does not yield satisfying results. The prognosis of the glioma pat ient depends more on the histological grading of the tumor and patient's ag e than on the therapy. Especially the adjuvant chemotherapy failed to date to influence survival time in glioma patients significantly. To improve res ults in malignant glioma therapy additional therapeutic regimes are necessa ry. In an earlier study we were able to show a significant reduction on perifoc al edema by an extract from gum resin (EGR) accompanied with a clinical imp rovement in patients with malignant glioma. Also a decrease of urinary LTE4 -excretion as a metabolite of leukotriene synthesis in brain tumors was obs erved. Furthermore we had found a proliferation inhibiting activity of the extract form EGR, the boswellic acids in cell cultures. The purpose of this experimental study was to elucidate the effects of the boswellic acids, which are constituents of an extract from gum resin on tum or growth in vivo. Female wistar rats weighing 200-250 g were treated with the drug 14 days after inoculation of C6 tumor cells into their right cauda te nucleus and randomization into 4 groups. The treatment groups received d ifferent dosages and were compared to a control group without any additiona l treatment. Survival time of the rats in the highest dosage group (3 x 240 mg/kg body weight) was more than twice as long as in the control group (P < 0.05). In a second experiment the inhibition of tumor cell proliferation was exami ned. The C6 tumor cells were implanted into the caudate nucleus. Drug treat ment was started immediately after implantation and stopped after 14 days. The animals were sacrificed and the brains were examined microscopically. C omparing low and high dosage of EGR treatment a significant difference in t umor volume was detected (P < 0.05). The proportion of apoptotic tumor cell s in animals with high dose treatment was significantly larger than in the low dose (treatment) group (P < 0.05). These data demonstrate an influence of EGR in rat glioma growth and might r epresent a new therapeutic option on glioma treatment in man in future. Fur ther experimental work on human gliomas is needed to definitively answer th is question.