Structure and Properties of Polysaccharides from &lt;i&gt;Viscum album&lt;/i&gt; (L.)

Sivamurthy

2017

Int J Pharm Pharm Sci

Objective: To find out the cytotoxicity, anti-tumor and anti-inflammatory activities of six species of plants belongs to Viscaeceae family available in Western Ghats (India).Methods: Cytotoxicity of Viscum extracts was studied by trypan blue exclusion and MTT assay using various cell lines. Anti-tumor activity was determined using Ehrlich ascites carcinoma (EAC) and Dalton's lymphoma ascites (DLA) cells in mice. Anti-inflammatory activities of Viscum extracts were studied using carrageenan and dextran induced mouse paw edema models. Results:Viscaeceae plant extracts studied were cytotoxic towards transformed cells DLA and EAC as well as to MCF-7, MDA-MB-231 and SKBR3 cell lines. Extracts of V. orientale, V. nepalense and V. ramosissimum, V. trilobatum were cytotoxic towards normal cells while V. angulatum and V. capitellatum were found to be nontoxic. Excepting V. angulatum all the other species selected here showed toxicity to animals. Administration of nontoxic concentration of extracts of Viscaeceae plants significantly (P<0.001) increased the lifespan of ascites tumor bearing animals and reduced DLA cells induced solid tumor development. All these plants except V. capitallatum and V. trilobatum showed significant (P<0.001) antiinflammatory activity against carrageenan and dextran models and reduced pro-inflammatory cytokine levels.Conclusion: Four plants of Viscum species studied were cytotoxic to tumour cells and inhibited tumour development. Of the six species studied V. angulatum was non-toxic to animals and showed maximum efficiency as an antitumour agent. These plants showed significant anti-inflammatory activity and reduced inflammatory markers.

Section: Introductionmentioning

confidence: 99%

Potential Anti-Tumor and Anti-Inflammatory Activity of Six Mistletoe Plants in the Family Viscaceae Present in Western Ghats, India

Sivamurthy

2017

Int J Pharm Pharm Sci

Cancer Immunol Immunother

“…Preliminary data suggested involvement of an arabinose derivative as an interacting group [30]. Polysaccharides, present in V. album extracts that might serve as a source for the active HM-BP component, have a complex structure containing rhamnogalacturonan, arabinogalactan and arabinan chains [16]. The lack of synergism of HM-BP and arabinogalactan (L. occidentalis) in activating NK cytotoxicity, as observed by us, may be taken as the first evidence for a common receptor, which possibly is also the target site for arabinogalactan from E. purpurea.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of stimulation of human natural killer cytotoxicity by arabinogalactan fromLarix occidentalis

Hauer

Anderer

1993

Cultures of human peripheral blood mononuclear cells (PBMC) as well as cultures of preseparated peripheral non-adherent cells (PNAC) and monocytes showed enhancement of natural killer (NK) cytotoxicity against K562 tumor cells when pretreated with arabinogalactan from Larix occidentalis for 48-72 h. Lack of enhanced responses of PBMC (37% of donors) did not necessarily mean that PNAC and monocyte cultures were also non-responsive to arabinogalactan treatment. Moreover, PBMC, PNAC and monocytes of individual donors could exhibit various responses to arabinogalactan when cultures derived from bleedings after intervals of several months were assayed. Arabinogalactan-mediated enhancement of NK cytotoxicity was not initiated directly but was found to be governed by the cytokine network. Generally, arabinogalactan pretreatment induced an increased release of interferon gamma (IFN gamma), tumor necrosis factor alpha, interleukin-1 beta (IL-1 beta) and IL-6 but only IFN gamma was involved in enhancement of NK cytotoxicity since cytotoxicity enhancement of PBMC and PNAC but not that of monocytes could be blocked when anti-IFN gamma antibodies were present during pretreatment. The presence of anti-IL-2 antibodies completely blocked NK cytotoxicity enhancement of PBMC and only moderately that of PNAC and monocytes. This blocking effect was also observed when no detectable increase of IL-2 release could be recorded. The receptor specificity of arabinogalactan is not well characterized. Initial information obtained from comparative studies indicated that arabinogalactan presumably interacts with a receptor that showed specificity for a NK-cytotoxicity-enhancing oligo-saccharide from Viscum album extracts since the action of both components was not synergistic but rather competitive.

Cancer Immunol Immunother

“…Preliminary data from work in progress indicate the involvement of an arabinose derivative as an interacting group. A polysaccharide present in V. album extract that might serve as a source for the active HM-BP component, has a complex structure containing rhamnogalacturonan, arabinogalactan and arabinan chains [ 18].…”

Section: Discussionmentioning

confidence: 99%

AViscum album oligosaccharide activating human natural cytotoxicity is an interferon γ inducer

1990

Commercial Viscum album extract Helixor-M contains a dialysable oligosaccharide (HM-BP) that activates natural killer (NK) cytotoxicity against K562 tumour cells when preincubated with human peripheral blood mononuclear cells (PBMC) for 72 h. The activated effector cells were exclusively found in the monocyte/macrophage subpopulation. However, when peripheral non-adherent cells (PNAC) were preincubated with HM-BP for 72 h the NK cytotoxicity of CD56+CD3- NK cells was activated. This discrepancy was found to be due to the release of prostaglandin E2 from activated monocytes/macrophages, which blocked activation of the cytotoxicity of NK cells. Analysis of the supernatant culture medium after 72 h preincubation demonstrated that HM-BP induced release of interferon gamma (IFN gamma) from T cells (preferentially from CD3+CD4+ cells) and of tumour necrosis factor alpha (TNF alpha) from monocytes/macrophages. Release of IFN gamma was the crucial step for activation of NK cytotoxicity since enhancement of NK cytotoxicity during pretreatment of PBMC or PNAC with HM-BP was completely blocked in the presence of anti-IFN gamma antibodies. Anti-interleukin-2, anti-TNF alpha or anti-IFN alpha antibodies had no effect on the HM-BP-induced enhancement of NK cytotoxicity. The activation of the NK cytotoxicity of nonadherent cells by interleukin-2 treatment was found to be synergistic to the enhancement of NK cytotoxicity by treatment with HM-BP.