DENDROPHTHOE PENTANDRA PDF

Mango Mistletoes (Dendrophthoe pentandra) is one type of mistletoe that It has been known that Dendrophtoe pentandra extract (DPE). Dendrophthoe pentandra. [Malayan Mistletoe]. Home. photo. DSC (11). photo. DSC (11). photo. DSC (14). photo. DSC (14). photo. Dendrophthoe pentandra (L.) Bl. Dendrophthoe pentandra (L.) Bl. Loranthus pentandrus L. Loranthus pentandrus L. Loranthus farinosus Desr. Loranthus.

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We have no special datasets in this article, the datasets supporting the conclusions of this article are included within this paper.

Indonesian mistletoe grows on various trees. Mango Mistletoes Dendrophthoe pentandra is one type of pentandea that grown on mango tree. Our study used mistletoe as a parasitic plant that has been used for traditional medicine. It has been known that Dendrophtoe pentandra extract DPE anti-inflammatory and anticancer. Furthermore, it is necessary to follow-up study in vivo to evaluate the response to treatment of new cancer therapeutic agents.

This study consists of five treatment groups: These findings indicate that the DPE could inhibit colonic epithelial cells proliferation through p53 pathway independently.

Dendrophthoe pentandra (L.) Miq.

This study also showed that DPE could be potential sources of new therapy. Since mistletoe is a semi-parasitic plant, it is suggests that their bioactivities could also depend on their host plant [ 1 ]. However people in Indonesia usually called the mistletoe depend on the host plant where it grew, such as benalu mangga mistletoe which used mango as host. DPE contains quercetinrhamnose [ 2 ].

Quercetin has anti-oxidant, anti-inflammatory, anti-cancer, and immune modulator effect [ 3 — 5 ]. Quercetin also improve the action of the drug 5-Fluorouracil 5-FU promoting increased expression of p53 and apoptosis in breast cancer T47D cells [ 67 ]. Colon cancer is caused by many factors that affect multiple etiological pathways.

Important risk factors include chronic inflammation, environmental effects and unhealthy lifestyle. All these risk factors are linked to cancer through inflammation [ 8 ]. Chronic inflammation in mice model that are initiated by the DSS causes colitis, deoxyribonucleic acid DNA damage and encourages the emergence of adenoma [ 1112 ].

That will lead CAC by increasing of cell signals, cell proliferation and suppressing of tumor suppressor and apoptosis [ 1314 ]. This CAC is associated with the cell cycle and its regulation is affected by the tumor suppressor proteins.

One of the tumor suppressor proteins such as p53 play an important role in the cell cycle and apoptosis. The function of p53 instead a transcription factor, targeting several genes that play a role in the cell cycle checkpoint and induction of apoptosis [ 1516 ]. Chronic inflammation causes the migration of inflammatory cells such as neutrophils. If the production of neutrophils is excessive, it will cause damage to tissue [ 17 ].

Interleukin binds ILR1 receptor complex, activates STAT3 [ 18 ] and encourage tissue repair to improve colonic epithelial cell proliferation in acute inflammatory conditions [ 19 ]. Interleukin is deregulated in cancer conditions, tissue regeneration regulation function is transformed into the driving cancer development [ 20 ].

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The mechanism of DPE as anti inflammation and proliferation still unknown. The plant was identified and authenticated by biologists in Department of Biology, University of Brawijaya specimen No.

The leaves were dried for five days at room temperature and then powdered. The filtrated was evaporated under reduced pressure to obtain of solid form of the extract. The quercetin content from DPE extraction was 0.

The mice were given normal drinking water ad libitum during the experimental periods. Mice have been fed with standard pellet and water ad libitum. Mice were given a single i.

Mice were randomly divided into five groups Fig. Control group received water vehicle. The administrated of DPE were started from the 8 th weeks until 21 th weeks. The activity of the enzyme myeloperoxidase MPO was used to assess further infiltration of neutrophils. E- El – M The cell proliferation patterns in the colon tissue were assessed by using BrdU immunohistochemistry. Briefly, paraffin-embedded colon tissue sections were deparaffinized and hydrated.

Incubations were performed in a humidified chamber. The tissue sections were sequentially incubated with biotinylated goat anti-mouse IgG no. Staining was developed with diaminobenzidine DAB; Sigma substrate and sections were counterstained with hematoxylin. Sections were evaluated using light microscopy and examined in a blind fashion by two individuals separately. The tissue fragments were re-suspended and incubated.

The incubation procedure was repeated for two times. After incubation, epithelial cells were washed with phosphate buffered saline PBSharvested by 0. Then, cells were permeabilized by 0. The amplification program consisted of the following steps: Based on previous studies, DSS was used in combination with AOM, received a chemical carcinogen which induces colorectal cancer in mice.

Blood in the feces was detected using an occult blood detection kit Hemoccult. Body growth rate was slightly lower in the mice that received DSS administration only Fig. IL levels were measured from supernatants of colon organ culture by enzyme linked immunosorbent assay. Each group consisted of at least four mice.

Dendrophthoe pentandra in Flora of China @

The DSS only group showed extensive ulceration, with severe inflammatory cell infiltration. The activity of the enzyme myeloperoxidase MPO was used to evaluate infiltration of neutrophils. MPO levels were measured from lysed colon cells.

This study, epithelial cells proliferation was observed by using anti-BrdU staining performed by Immunohistochemistry. The microscopic appearance of colonic epithelial cells of CAC mice model showed undergo proliferation pentanxra DSS only group.

Administration of DPE dendrophtboe decreased proliferation of epithelial cells. In this study, DPE suppressed carsinogenesis by reducing the proliferation of epithelial cells. Colonic proliferation cells from the colon CAC mice models. Epithelial proliferation enhanced in colon of CAC mice model. Colon tissues were treated with anti BrDu antibody counterstained with hematoxylin and visualized under the light microscope.

Cell proliferation identified by BrdU immunohistochemical staining of paraffin section. Brown-color nucleus indicates BrdU-positive cells.

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All images were magnified at x and representative four independent experiments with consistent results.

Number of BrdU positive cells. We examined whether colonic epithelial cells were resting or proliferating state. DNA synthesis was measured in colonic epithelial cells followed. The percentage of BrdU-labeled S-phase cells were determined by observing labeled cells undergoing of the S-phase of the cell cycle. Induction of DPE treatment change the percentage of cells in S phase through not in a dose dependent manner.

Cell cycle analysis of colonic epithelial cells treated with or without DPE. Data are representative of four independent experiments with similar results. B The percentage of cells in S phase. The expression of p53 responded to administration of DPE in a manner inversely doses dependent.

Relative gene expression of p53 from the colon of CAC models. Results are representative of four independent experiments.

Thus, in our study, DPE administration led to a significant reduction of proliferation, which was accompanied by decreased IL, so that it would be capable of suppressing the pentamdra of CAC. This result is consistent with the report that D. The results of the current study indicated that the ability of mice to develop CAC was inhibited by the administration of the DPE treatment.

This finding suggests that DPE treated mice were protected from inflammation. Neutrophils would amplify inflammation by secreting enzyme myeloperoxidase MPO to release the inflammatory mediators. It has been known that DPE contains quercetin, a compound that has function as inflammation inhibitor [ dencrophthoe ] by blocking phosphorylation inhibitors Kappa B IKB [ 3426 ].

Our results show that DPE treatment causes G1 arrest of cell cycle. This study demonstrated that DPE treatment induce cell cycle inhibition in S phases.

Here we show that DPE treatment impedes S-phase. This led to an examination of the molecular mechanisms of cell cycle regulation by DPE.

A prominent cell cycle arrest at S phase was noted upon treatment with quercetin [ 27 ]. Besides, an reduce of cells in S phase was observed in DPE administration.

This suggests that quercetin might restrain DNA synthesis. Our results indicate that DPE induced pmediated inhibition of S phase in cell cycle. Pentanera tumor suppressor protein p53 plays a central role in cancer prevention and therapy. The regulation of p53 occurs in cell cycle in a variety of cells [ 3031 ]. In addition, DPE has up-regulated p53 function and progression at the S cell cycle phase.

DPE promoted DNA synthesis as indicated by the lack presentation of S phase, and they were functionally able to suppress the development of proliferation. Meanwhile, DPE in high doses may cause increased risk of toxicity. This finding suggested that the accumulation of toxic substances could effects of p53 expression.