Frankincense oil

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frankincense essential oil

What is frankincense oil

Frankincense essential oil is prepared by the steam distillation of frankincense gum resin (olibanum) is one of the most commonly used essential oils in aromatherapy. Frankincense is an aromatic resin hardened from exuded gums obtained from trees of the genus Boswellia (Burseraceae family). Boswellia species includes Boswellia sacra from Oman and Yemen, Boswellia carteri from Somalia, and Boswellia serrata from India and China 1. The frankincense gum resin (olibanum) has been used in incense and fumigants, as well as a fixative in perfumes. Aroma from these resins is valued for its superior qualities for religious rituals since the time of ancient Egyptians 2. Boswellia species resins have also been considered throughout the ages to have a wealth of healing properties. Considerable amount of work has been attempted to identify chemical compositions of frankincense essential oils from different commercial brands. Chemical constituents of frankincense essential oils differ significantly due to climates, time of harvest, storage conditions, geographical sources of resins 3, and methods of preparations. The frankincense essential oil has been demonstrated in test tube studies to modulate critical biological activities including anti-rheumatism, anti-inflammatory 4, antibacterial, antifungal and anticancer activities 5. Boswellic acids from frankincense gum resins have been suggested to be a major compound in mediating various biological functions including anti-inflammatory and anti-cancer activities. Chevrier et al. 6 reported that ethanol extracts of Boswellia carteri gum resins comprise 7 boswellic acids. Akihisa et al. 7 reported that methanol extracts of Boswellia carteri resins consist of 15 triterpene acids including boswellic acids. Acetyl-11-keto-β-boswellic acid (AKBA) provides protective effects in a chemically induced mouse ulcerative colitis model 8. It has been shown that β-boswellic acids from methanol extracts of Boswellia cateri gum resins exhibit potent cytotoxic activities against human neuroblastoma cell lines, IMR-32, NB-39, and SK-N-SH 7. Shao et al. 9 compared 4 triterpene acids including β-boswellic acid, 3-O-acetyl-β-boswellic acid and acetyl-11-keto-β-boswellic acid (AKBA) isolated from Boswellia serrata gum resins for their anti-cancer activity in vitro. Acetyl-11-keto-β-boswellic acid (AKBA) is the most pronounced inhibitory effects among the 4 triterpene acids in suppressing human leukemia HL-60 cell growth as well as DNA, RNA, and protein synthesis 9. AKBA also exhibits anti-proliferative and pro-apoptotic activities against human prostate cancer LNCaP and PC-3 cells in vitro and in animal models 10, and induces cytotoxicity in human meningioma cells in culture 11. Acetyl-11-keto-β-boswellic acid (AKBA) have also been proposed to provide anti-neoploastic activity through their anti-proliferative and pro-apoptotic properties in multiple human cancer cell lines including hepatoma cells 12, melanoma cells 13, fibrosarcoma cells 13, colon cancer cells 14, pancreatic cancer cells 15 and prostate cancer cells 16. Moreover, boswellic acids may not be the only compounds in frankincense essential oil for inducing pancreatic cancer cell death. Total boswellic acids contents were not proportionally related to essential oil-induced tumor cell cytotoxicity among different fractions. Additionally, frankincense hydrosol, the aqueous distillate of hydrodistilled Boswellia sacra gum resins, contained 0.0 to 15.5% boswellic acids, but did not have detectible cytoxicity against tumor cells even when a 1:5 dilution was added to the cultures. Tirucallic acids purified from Boswellia carteri gum resins have been shown to induce human prostate cancer cells death 17. Some researchers also observed that frankincense essential oil enriched with high molecular weight compounds but lower boswellic acids contents frankincense essential oil was much more potent at inducing cytotoxicity in cultured pancreatic cancer cells.

Higher boswellic acids contents are present in frankincense essential oil hydrodistilled at higher temperature. A study by Hostanska et al. 18 reported that components other than AKBA from solvent extracts of Boswellia serrata gum resins can induce cytotoxicity in malignant cells. Additionally, Estrada et al. 19 reported that tirucallic acids purified from Boswellia carteri gum resins induce apoptosis in human prostate cancer cell lines. Although the active compound(s) in Boswellia sacra frankincense essential oil responsible for anti-tumor activity cannot be identified immediately due the complexity of frankincense essential oils, chemical compositions and/or ratios of these components present in the oil obtained at 100 °C (212 °F) would play significant roles in tumor cell-specific cytotoxicity.

Frankincense essential oil-regulated cell cycle regulators and signaling pathways were compared to boswellia acids-activated pathways in a variety of cancer cell lines. It has been reported that boswellic acids can regulate tumor cell viability by activating a variety of mechanisms. Acetyl-keto-beta-boswellic acid (AKBA) arrests cancer cells at the G1 phase of cell cycle, suppresses levels of cyclin D1 and E, cdk 2 and 4, and Rb phosphorylation, as well as increases expression of p21 through a p53-independent pathway 20. Acetyl-keto-beta-boswellic acid (AKBA) activates death receptor-5 through elevated expression of CATT/enhancer binding protein homologus protein in human prostate cancer LNCaP and PC-3 cells 21. Boswellic acids including AKBA strongly induce apoptosis through activation of caspase-3, -8, and −9 and cleavages of PARP in colon cancer HT29 cells and hepatoma HepG2 cells 22. In addition, AKBA inhibits topoisomerases I and II without inhibiting DNA fragmentation in glioma and leukemia HL-60 cells 23.

Boswellia sacra essential oil also suppresses important malignant features of tumor cells, such as invasion and multicellular tumor spheroids growth. Tumor cell plasticity enables highly malignant tumor cells to express endothelial cell-specific markers and form vessel-like network structures on basement membranes. The in vitro Matrigel-based tumor invasion model has been shown to correlate with in vivo metastatic potential 24. This in vitro model has been used to study mechanisms of cancer aggressive behavior, metastasis, and poor prognosis 25, and has been used as a tool to screen therapeutic agents for their anti-metastatic property 26. Boswellia sacra frankincense essential oil obtained at 100 °C (212 °F) is more potent than essential oil obtained at 78 °C hydrodistillation in disruption cellular networks on Matrigel and spheroids. More importantly, observations obtained in the above described experimental models are consistent with clinical responses in human cancer cases. These results suggest that Boswellia sacra frankincense essential oil may represent an effective therapeutic agent for treating invasive breast cancer. The anti-tumor activity of frankincense essential oil is mediated through multiple signaling pathways and cell cycle regulators. To further confirm these anti-cancer and other therapeutic activities of frankincense essential oil and frankincense resin extracts which are derived from animal and test tube studies, human clinical studies are required to support their uses in human diseases. Currently, a Boswellia serrata extracts is undergoing a phase I trial to study how well Boswellia serrata extract works in treating patients with ductal breast carcinoma in situ, stage I-III breast cancer, or stage I-III colon cancer that are undergoing surgery 27.

Frankincense essential oil uses and benefits

In traditional Chinese medicine, frankincense from Boswellia carterii is commonly used for topical treatment of pain and inflammation 28. A study carried out to investigate the antinociceptive and anti-inflammatory action of frankincense oil and water extracts and three of its main componentes, i.e., linalool, α-pinene and 1-octanol, via xylene-induced ear edema and a formalin-inflamed hindpaw model in male Kunming mice, showed consistent evidence about their anti-inflammatory and analgesic effects. Frankincense oil extract, which contains more linalool, α-pinene and 1-octanol than frankincense water extract, produced a faster and more effective reduction of the swelling and pain than the water extract 29. In addition, the combination of linalool, α-pinene and 1-octanol exhibited stronger biological effect on hindpaw inflammation and cyclooxygenase-2 (COX-2) overexpression than the three compounds used separately, indicating that they contribute to the topical antinociceptive and anti-inflammatory properties of frankincense by inhibiting cyclooxygenase-2 (COX-2) activation 30. For example, resins of Boswellia species have been used for the treatment of rheumatoid arthritis and other inflammatory diseases 31 such as Crohn’s disease 32. The anti-inflammatory activity has been attributed to the frankincense gum resin’s ability in regulating immune cytokine production 6 and leukocyte infiltration 33.

In a well conducted systematic study by Cochrane researchers 34 comparing Boswellia serrata extract, bismuth subsalicylate (Pepto-Bismol®), mesalamine, cholestyramine, probiotics, prednisolone and budesonide therapy in collagenous colitis – a type of microscopic colitis, a condition characterized by chronic watery non-bloody diarrhea. People with collagenous colitis have a normal appearing bowel when assessed by an endoscope (a camera used to look at the bowel); but have microscopic inflammation of the bowel when assessed by a biopsy (a tissue sample taken during endoscopy). The cause of this disorder is unknown. Budesonide is an immunosuppressive steroid drug that is quickly metabolized by the liver resulting in reduced steroid-related side-effects. Prednisolone is a steroid drug used to treat inflammation. Mesalamine (also known as 5-ASA) is an anti-inflammatory drug. Cholestyramine is a drug that helps the body remove bile acids. Pepto-Bismol®, is an antacid medication used to treat discomforts of the stomach and gastrointestinal tract. Probiotics are found in yogurt or dietary supplements and contain potentially beneficial bacteria or yeast. The researchers investigated whether these treatments improve symptoms (e.g. diarrhea) or microscopic inflammation of collagenous colitis and whether any side effects (harms) result from treatment. The outcome of that Cochrane review 34 was there is a low quality evidence suggesting that budesonide may be effective for inducing and maintaining clinical and histological response in patients with collagenous colitis. Furthermore, due to small sample sizes and low study quality, the study authros were uncertain about the benefits and harms of therapy with Pepto-Bismol®, Boswellia serrata extract, mesalamine with or without cholestramine, prednisolone and probiotics. These agents and other therapies require further study.

Madisch 2007 35 completed a randomized, placebo-controlled, double-blind study at multiple German centers to evaluate the clinical response of Boswellia serrata extract on patients with collagenous colitis compared to placebo over 6 weeks. Thirty-one patients (aged 18 to 80 years) with clinically and histologically confirmed collagenous colitis (“at least five liquid or soft stools per day on average per week, and a complete colonoscopy performed within the last 4 weeks before randomization”) were randomized to receive Boswellia serrata extract (three 400 mg/day; n = 16) or identically matched placebo (n = 15). Patients were excluded in they had received budesonide, salicylates, steroids, prokinetics, antibiotics, ketoconazole, or non-steroidal anti-inflammatory drugs within four weeks of randomization or if they had other endoscopically or histologically verified causes for diarrhea, infectious diarrhea, previous colonic surgery, or known intolerance to Boswellia serrata extract or were pregnant or lactating. The primary endpoint was clinical remission after 6 weeks (stool frequency of < 3 per day); secondary outcomes included histological improvements and quality of life measures. “Patients who did not respond to treatment after 6 weeks were individually unblinded. If they were in the active treatment group, they were judged as treatment failure. If they were in the placebo group, crossover therapy with open-labelled Boswellia serrata extract 400 mg, given orally three times daily was offered.” Intention to treat analysis demonstrated no significant effect of Boswellia serrata extract compared to placebo on achieving clinical remission, 43.8% vs 26.7%, respectively) 35. In Madisch 2007 35, there was a slight reduction in the thickness of the subepithelial collagen band and inflammation score in both the Boswellia serrata and placebo groups at the end of 6 weeks of therapy, but no difference compared to baseline or between the groups. At the end of 6 weeks of therapy, there were no significant changes in quality of life scores in either the Boswellia serrata or placebo groups compared to baseline or between groups 35.

In another 2014 Cochrane review 36 involving oral herbal therapies for treating osteoarthritis. Thirty-three different medicinal plant products were compared with placebo or active intervention controls and many comparisons had single studies only; the authors have restricted reporting of results to multiple studies of Boswellia serrata (monoherbal) and avocado-soyabean unsaponifiables (ASU) (two herb combination) products. The authors’ conclusions were there was evidence for the proprietary avocado-soyabean unsaponifiables (ASU) product Piasclidine® in the treatment of osteoarthritis symptoms seems moderate for short term use, but studies over a longer term and against an apparently active control are less convincing. Several other medicinal plant products, including extracts of Boswellia serrata, have moderate-quality evidence for trends of benefits that warrant further investigation in light of the fact that the risk of adverse events appear low 36.

There is no evidence that Piasclidine® significantly improves joint structure, and limited evidence that it prevents joint space narrowing. Structural changes were not tested for with any other herbal intervention 36.

Further investigations are required to determine optimum daily doses producing clinical benefits without adverse events 36.

Key results of the oral herbal therapies for treating osteoarthritis 36:

Boswellia serrata

Pain on a scale of 0 to 100 points (lower scores mean reduced pain):

  • people who used 100 mg of enriched Boswellia serrata extract rated their pain 17 points lower (range 8 to 26 points lower) (17% absolute improvement) at 90 days compared with placebo;
  • people who used enriched Boswellia serrata extract 100 mg rated their pain as 23 points;
  • people who used a placebo preparation rated their pain as 40 points.

Physical function on a scale of 0 to 100 points (lower scores means better physical function):

  • people who used 100 mg of enriched Boswellia serrata extract rated their physical function 8 points better (2 to 14 points better) on a 100 point scale (8% absolute improvement) at 90 days compared with placebo;
  • people who used 100 mg of enriched Boswellia serrata extract rated their physical function as 25 points;
  • people who used placebo rated their physical function as 33 points.

Avocado-soyabean unsaponifiables (ASU) product Piascledine®

Pain on a scale of 0 to 100 points (lower scores mean less pain):

  • people who used avocado-soyabean unsaponifiables 300 mg rated their pain 8 points lower (1 to 16 points lower) on a 100 point scale (8% absolute improvement) at 3 to 12 months compared with placebo;
  • people who used avocado-soyabean unsaponifiables 300 mg rated their pain as 33 points;
  • people who used placebo rated their pain as 41 points.

Physical function on a scale of 0 to 100 mm scale (lower scores means better physical function):

  • people who used avocado-soyabean unsaponifiables 300 mg rated their physical function 7 mm better (2 to 12 mm better) on a 100 mm scale (7% absolute improvement) at 3 to 12 months compared with placebo;
  • people who used avocado-soyabean unsaponifiables 300 mg rated their physical function as 40 mm;
  • people who used placebo rated their physical function as 47 mm.

Summary and quality of the evidence

There is moderate-quality evidence that in people with osteoarthritis Boswellia serrata slightly improved pain and function. Further research may change the estimates.

There is moderate-quality evidence that avocado-soybean unsaponifiables (ASU) probably improved pain and function slightly, but may not preserve joint space. Further research may change the estimates.

The study authors were uncertain whether other oral herbal products improve osteoarthritis pain or function, or slow progression of joint structure damage because the available evidence is limited to single studies or studies that cannot be pooled, and some of these studies are of low to very low quality. Quality of life was not measured.

Herbal therapies may cause side effects, however they were uncertain if there is an increased risk of these.

Figure 1. Frankincense gum resin

Figure 2. Frankincense essential oil

Frankincense oil side effects

There is only little published material as far as side effects are concerned. In the clinical trials described in this study 37, two out of 40 patients who received frankincense gum resin of 300 mg three times daily over a period of 6 weeks complained about epigastric pain, hyperacidity and nausea 38. In the study dealing with ulcerative colitis 39, 6 out of 34 patients complained about retrosternal burning, nausea, fullness of abdomen, epigastric pain and anorexia. In a study reported by Böker et al. 40, some patients developed nausea and vomiting, in two patients skin irritations have also been observed. The side effects were reversible after omission of the treatment. In the study of Streffer et al. 41, some gastrointestinal symptoms were observed.

In a retrospective analysis in 2000, the laboratory parameters before and after treatment of patients suffering from rheumatoid arthritis, ulcerative colitis, Crohn’s disease, neurodermitis, lupus erythematosus, multiple sclerosis, astrocytoma, glioblastoma, bronchial asthma and psoriasis and receiving the Boswellia preparation H15TM over a period of 6 years before and after treatment were tested. No significant changes related to the therapy were observed 42.

In Madisch 2007 35 randomized, placebo-controlled, double-blind study at multiple German centers to evaluate the clinical response of Boswellia serrata extract on patients with collagenous colitis compared to placebo over 6 weeks, 12.5% (2/16) of patients treated with Boswellia serrata extract reported an adverse event. Of these, 1 patient withdrew from the trial due to hypoglycemia, dizziness and anorexia. The other developed bacterial enteritis but completed the trial. One of 15 patients (7%) in the placebo group reported an adverse event (eczema and Coxsackie virus infection), but completed the trial. There was no significant different between the groups in adverse events or withdrawals due to adverse events. Twelve per cent (2/16) of patients treated with Boswellia serrata extract had an adverse event compared to 7% (1/15) of patients treated with placebo. Six (1/16) of patients treated with Boswellia serrata extract withdrew due to an adverse event compared to 0% (0/15) of patients treated with placebo. None of the adverse events were considered serious.

  1. Suhail MM, Wu W, Cao A, et al. Boswellia sacra essential oil induces tumor cell-specific apoptosis and suppresses tumor aggressiveness in cultured human breast cancer cells. BMC Complementary and Alternative Medicine. 2011;11:129. doi:10.1186/1472-6882-11-129. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258268/[↩]
  2. Maloney GA. Gold, frankincense, and myrrh : an introduction to Eastern Christian spirituality. New York: Crossroads Pub. Co; 1997.[↩]
  3. Chemistry and immunomodulatory activity of frankincense oil. Mikhaeil BR, Maatooq GT, Badria FA, Amer MM. Z Naturforsch C. 2003 Mar-Apr; 58(3-4):230-8. https://www.ncbi.nlm.nih.gov/pubmed/12710734/[↩]
  4. Poeckel D, Werz O. Boswellic acids: Biological actions and molecular targets. Curr Med Chem. 2006;13:3359–3369. doi: 10.2174/092986706779010333. http://www.eurekaselect.com/58250/article[↩]
  5. Syrovets T, Büchele B, Krauss C, Laumonnier Y, Simmet T. Acetyl-boswellic acids inhibit lipopolysaccharide-mediated TNF-alpha induction in monocytes by direct interaction with IkappaB kinases. J Immunol. 2005;174:498–506. doi: 10.4049/jimmunol.174.1.498. http://www.jimmunol.org/content/174/1/498.long[↩]
  6. Chevrier MR, Ryan AE, Lee DY, Zhongze M, Wu-Yan Z, Via CS. Boswellia carterii extract inhibits TH1 cytokines and promotes TH2 cytokines in vitro. Clin Diagn Lab Immunol. 2005;12:575–580. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1112084/[↩][↩]
  7. Akihisa T, Tabata K, Banno N, Tokuda H, Nishimura R, Nakamura Y, Kimura Y, Yasukawa K, Suzuki T. Cancer chemopreventive effects and cytotoxic activities of the triterpene acids from the resin of Boswellia carteri. Biol Pharm Bull. 2006;29:1976–1979. doi: 10.1248/bpb.29.1976. https://www.ncbi.nlm.nih.gov/pubmed/16946522[↩][↩]
  8. Anthoni C, Laukoetter MG, Rijcken E, Vowinkel T, Mennigen R, Muller S, Senninger N, Russell J, Jauch J, Bergmann J. et al. Mechanisms underlying the anti-inflammatory actions of boswellic acid derivatives in experimental colitis. Am J Physiol Gastrointest Liver Physiol. 2006;290:G1131–1137. doi: 10.1152/ajpgi.00562.2005. https://www.ncbi.nlm.nih.gov/pubmed/16423918[↩]
  9. Shao Y, Ho CT, Chin CK, Badmaev V, Ma W, Huang MT. Inhibitory activity of boswellic acids from Boswellia serrata against human leukemia HL-60 cells in culture. Planta Med. 1998;64:328–331. doi: 10.1055/s-2006-957444. https://www.ncbi.nlm.nih.gov/pubmed/9619114[↩][↩]
  10. Lu M, Xia L, Hua H, Jing Y. Acetyl-keto-β-boswellic acid induces apoptosis through a death receptor 5-mediated pathway in prostate cancer cells. Cancer Res. 2008;68:1180–1186. doi: 10.1158/0008-5472.CAN-07-2978. http://cancerres.aacrjournals.org/content/68/4/1180.long[↩]
  11. Park YS, Lee JH, Bondar J, Harwalkar JA, Safayhi H, Golubic M. Cytotoxic action of acetyl-11-keto-β-boswellic acid (AKBA) on meningioma cells. Planta Med. 2002;68:397–401. doi: 10.1055/s-2002-32090. https://www.ncbi.nlm.nih.gov/pubmed/12058313[↩]
  12. Liu JJ, Nilsson A, Oredsson S, Badmaev V, Duan RD. Keto- and acetyl-keto-boswellic acids inhibit proliferation and induce apoptosis in Hep G2 cells via a caspase-8 dependent pathway. Int J Mol Med. 2002;10:501–505. https://www.ncbi.nlm.nih.gov/pubmed/12239601[↩]
  13. Zhao W, Entschladen F, Liu H, Niggemann B, Fang Q, Zaenker KS, Han R. Boswellic acid acetate induces differentiation and apoptosis in highly metastatic melanoma and fibrosarcoma cells. Cancer Detect Prev. 2003;27:67–75. doi: 10.1016/S0361-090X(02)00170-8. https://www.ncbi.nlm.nih.gov/pubmed/12600419[↩][↩]
  14. Liu JJ, Nilsson A, Oredsson S, Badmaev V, Zhao WZ, Duan RD. Boswellic acids trigger apoptosis via a pathway dependent on caspase-8 activation but independent on Fas/Fas ligand interaction in colon cancer HT-29 cells. Carcinogenesis. 2002;23:2087–2093. doi: 10.1093/carcin/23.12.2087. https://www.ncbi.nlm.nih.gov/pubmed/12507932[↩]
  15. Boswellic acid suppresses growth and metastasis of human pancreatic tumors in an orthotopic nude mouse model through modulation of multiple targets. Park B, Prasad S, Yadav V, Sung B, Aggarwal BB. PLoS One. 2011; 6(10):e26943.[↩]
  16. Pang X, Yi Z, Zhang X, Sung B, Qu W, Lian X, Aggarwal BB, Liu M. Acetyl-11-keto-b-boswellic acid inhibits prostate tumor growth by suppressing vascular endothelial growth factor receptor 2-mediated angiogenesis. Cancer Res. 2009;69:5893–5900. doi: 10.1158/0008-5472.CAN-09-0755. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2724674/[↩]
  17. Tirucallic acids are novel pleckstrin homology domain-dependent Akt inhibitors inducing apoptosis in prostate cancer cells. Estrada AC, Syrovets T, Pitterle K, Lunov O, Büchele B, Schimana-Pfeifer J, Schmidt T, Morad SA, Simmet T. Mol Pharmacol. 2010 Mar; 77(3):378-87. http://molpharm.aspetjournals.org/content/77/3/378.long[↩]
  18. Hostanska K, Daum G, Saller R. Cytostatic and apoptosis-inducing activity of boswellic acids toward malignant cell lines in vitro. Anticancer Res. 2002;22:2853–2862. https://www.ncbi.nlm.nih.gov/pubmed/12530009[↩]
  19. Estrada AC, Syrovets T, Pitterle K, Lunov O, Buchele B, Schimana-Pfeifer J, Schmidt T, Morad SA, Simmet T. Tirucallic acids are novel pleckstrin homology domain-dependent Akt inhibitors inducing apoptosis in prostate cancer cells. Mol Pharmacol. 2010;77:378–387. doi: 10.1124/mol.109.060475. http://molpharm.aspetjournals.org/content/77/3/378.long[↩]
  20. Acetyl-keto-beta-boswellic acid inhibits cellular proliferation through a p21-dependent pathway in colon cancer cells. Liu JJ, Huang B, Hooi SC. Br J Pharmacol. 2006 Aug; 148(8):1099-107. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1752013/[↩]
  21. Acetyl-keto-beta-boswellic acid induces apoptosis through a death receptor 5-mediated pathway in prostate cancer cells. Lu M, Xia L, Hua H, Jing Y. Cancer Res. 2008 Feb 15; 68(4):1180-6. http://cancerres.aacrjournals.org/content/68/4/1180.long[↩]
  22. Keto- and acetyl-keto-boswellic acids inhibit proliferation and induce apoptosis in Hep G2 cells via a caspase-8 dependent pathway. Liu JJ, Nilsson A, Oredsson S, Badmaev V, Duan RD. Int J Mol Med. 2002 Oct; 10(4):501-5. https://www.ncbi.nlm.nih.gov/pubmed/12239601/[↩]
  23. Acetyl-11-keto-beta-boswellic acid induces apoptosis in HL-60 and CCRF-CEM cells and inhibits topoisomerase I. Hoernlein RF, Orlikowsky T, Zehrer C, Niethammer D, Sailer ER, Simmet T, Dannecker GE, Ammon HP. J Pharmacol Exp Ther. 1999 Feb; 288(2):613-9. http://jpet.aspetjournals.org/content/288/2/613.long[↩]
  24. Feng X, Wu Z, Wu Y, Hankey W, Prior TW, Li L, Ganju RK, Shen R, Zou X. Cdc25A regulates matrix metalloprotease 1 through Foxo1 and mediates metastasis of breast cancer cells. Mol Cell Biol. 2011;31:3457–3471. doi: 10.1128/MCB.05523-11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3147788/[↩]
  25. Flavin DF. A lipoxygenase inhibitor in breast cancer brain metastases. J Neurooncol. 2007;82:91–93. doi: 10.1007/s11060-006-9248-4. Gozgit JM, Pentecost BT, Marconi SA, Otis CN, Wu C, Arcaro KF. Use of an aggressive MCF-7 cell line variant, TMX2-28, to study cell invasion in breast cancer. Mol Cancer Res. 2006;4:905–913. doi: 10.1158/1541-7786.MCR-06-0147 http://mcr.aacrjournals.org/content/4/12/905.long[↩]
  26. Liang Z, Wu T, Lou H, Yu X, Taichman RS, Lau SK, Nie S, Umbreit J, Shim H. Inhibition of breast cancer metastasis by selective synthetic polypeptide against CXCR4. Cancer Res. 2004;64:4302–4308. doi: 10.1158/0008-5472.CAN-03-3958. http://cancerres.aacrjournals.org/content/64/12/4302.long[↩]
  27. Boswellia Serrata Extract in Treating Patients with Ductal Breast Carcinoma In Situ, Stage I-III Breast Cancer, or Stage I-III Colon Cancer That Are Undergoing Surgery. https://www.cancer.gov/about-cancer/treatment/clinical-trials/search/v?id=NCI-2017-01671&r=1[↩]
  28. Analgesic effects of crude extracts and fractions of Omani frankincense obtained from traditional medicinal plant Boswellia sacra on animal models. Al-Harrasi A, Ali L, Hussain J, Rehman NU, Mehjabeen, Ahmed M, Al-Rawahi A. Asian Pac J Trop Med. 2014 Sep; 7S1():S485-90. https://www.ncbi.nlm.nih.gov/pubmed/25312172/[↩]
  29. De Cássia da Silveira e Sá R, Lima TC, da Nóbrega FR, de Brito AEM, de Sousa DP. Analgesic-Like Activity of Essential Oil Constituents: An Update. International Journal of Molecular Sciences. 2017;18(12):2392. doi:10.3390/ijms18122392. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5751100/[↩]
  30. Li X.J., Yang Y.J., Li Y.S., Zhang W.K., Tang H.B. α-Pinene, linalool, and1-octanol contribute to the topical anti-inflammatory and analgesic activities of frankincense by inhibiting COX-2. J. Ethnopharmacol. 2016;179:22–26. doi: 10.1016/j.jep.2015.12.039. https://www.ncbi.nlm.nih.gov/pubmed/26721216[↩]
  31. Banno N, Akihisa T, Yasukawa K, Tokuda H, Tabata K, Nakamura Y, Nishimura R, Kimura Y, Suzuki T. Anti-inflammatory activities of the triterpene acids from the resin of Boswellia carteri. J Ethnopharmacol. 2006;107:249–253. doi: 10.1016/j.jep.2006.03.006. https://www.ncbi.nlm.nih.gov/pubmed/16621377[↩]
  32. Langmead L, Rampton DS. Review article: complementary and alternative therapies for inflammatory bowel disease. Aliment Pharmacol Ther. 2006;23:341–349. doi: 10.1111/j.1365-2036.2006.02761.x. https://www.ncbi.nlm.nih.gov/pubmed/16422993[↩]
  33. Sharma ML, Khajuria A, Kaul A, Singh S, Singh GB, Atal CK. Effect of salai guggal ex-Boswellia serrata on cellular and humoral immune responses and leucocyte migration. Agents Actions. 1988;24:161–164. doi: 10.1007/BF01968095 https://www.ncbi.nlm.nih.gov/pubmed/3407547[↩]
  34. Kafil TS, Nguyen TM, Patton PH, MacDonald JK, Chande N, McDonald JWD. Interventions for treating collagenous colitis. Cochrane Database of Systematic Reviews 2017, Issue 11. Art. No.: CD003575. DOI: 10.1002/14651858.CD003575.pub6. http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD003575.pub6/full[↩][↩]
  35. Madisch A, Miehlke S, Eichele O, Mrwa J, Bethke B, Kuhlisch E, et al. Boswellia serrata extract for the treatment of collagenous colitis. A double-blind, randomized, placebo-controlled multicenter trial. International Journal of Colorectal Disease 2007;22(12):1445-51.[↩][↩][↩][↩][↩]
  36. Cameron M, Chrubasik S. Oral herbal therapies for treating osteoarthritis. Cochrane Database of Systematic Reviews 2014, Issue 5. Art. No.: CD002947. DOI: 10.1002/14651858.CD002947.pub2 http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD002947.pub2/full[↩][↩][↩][↩][↩]
  37. Boswellic Acids in Chronic Inflammatory Diseases. Planta Med 2006; 72(12): 1100-1116. https://www.thieme-connect.com/products/ejournals/html/10.1055/s-2006-947227[↩]
  38. Gerhardt H, Seifert F, Buvari P, Vogelsang H, Repges R Z. Therapie des aktiven Morbus Crohn mit Boswellia serrata Extract H 15. Z Gastroenterol. 2001; 39 11-7[↩]
  39. Peskar E M. Inhibition of intestinal leukotriene formation as a possible mechanism of action of sulfosalazine, 5-aminosalicylic acid and 4-aminosalicylic acid. Klin Wochenschr. 1988; 66 1147-50[↩]
  40. Böker D K, Winking M. Die Rolle von Boswellia-Säuren in der Therapie maligner Gliome. Dtsch Ärztebl. 1997; 94 B-958 – 60[↩]
  41. Streffer J R, Bitzer M, Schabet M, Dichgans J, Weller M. Response of radiochemotherapy-associated cerebral edema a phytotherapeutic agent, H15. Neurology. 2001; 56 1219-21[↩]
  42. Buvari P G. Wirksamkeit und Unbedenklichkeit der H15 Ayurmedica-Therapie bei chronisch entzündlichen Erkrankungen [dissertation]. Mannheim-Heidelberg; University of Mannheim-Heidelberg 2001[↩]

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