kajian saintifik mengenai taheebo

Bagaimanakah unsur2 dalam “taheebo life tea” membunuh sel kanser?

Soalan ini ditanya olih pembaca web saya baru2 ini.

Banyak kajian saintifik sebenarnya telah dilakukan mengenai tindakbalas

“beta lapachone” ( nama kimia bagi taheebo ) terhada sel kanser.

Kajian sains mengatakan sel kita melalui sautu proses yang dinamakan ” OPOPTOSIS”

Ia merupakan proses semulajadi,ia itu proses menghapuskan sel2 yang tidak diperlukan

olih sistem badan seperti sel2 yang rosak dan sel2 yang berlebihan.Satu isyarat akan

dihantar kepada sel2 ini untuk melakukan “kamikaze” kerana sesuatu keperluan

seperti bercambahnya sel kanser.Bahkan ada pendapat ahli sains mengatakan jika

sel2 ini gagal melakukan “kamikazi” sautu pilihan lain ialah membungkus sel2 kanser

ini dengan lapisan2 sel pelindung yang dihantar olih sistem badan.Dan ini dinamakan

“lumps”.Ia penting untuk mengelakkan sel2 kanser ini dari menular ke tisu2 berhampiran.

Sebenarnya isyarat “opoptosis”  dihantar dalam peringkat awal dimana sistem badan

mengesan unsur2  sesutu sel itu bakal bertukar menjadi sel kanser.isyarat ini dikenali sebagai  protin53 atau p53.

Memandangkan sel kanser tidak berhubung dengan sistem otak,badan

sebenarnya bergantung kepada p53 untuk menentukan samada sesuatu

itu akan bertukar menjadi kanser atau tidak.Namun pada sesetengah

keadaan  pengaktifan isyarat p53 ini tidak  berfungsi.Ini akan menyebabkan seseorang

itu akan mendapat kanser.Diantara sebab2 isyarat p53 ini

gagal berfungsi ialah faktor genetik dimana terdapat rmai dari keturunan

seseorang itu mengidap kanser.Faktor2 lain ialah serangan virus

atau jangkitan bakteria.

Sila baca lapuran mengenai “beta lapachone” keatas sel kanser yang dibuat olih ahli sains Korea.

Lee JI, Choi DY, Chung HS, Seo HG, Woo HJ, Choi BT, Choi YH. R&E Program, Korea Science Academy, Busan, South Korea.

Abstract

AIM: To study in vitro the molecular mechanism of apoptosis caused by beta-lapachone, a quinone obtained from the bark of the lapacho tree (Tabebuia avellanedae).

MATERIALS AND METHODS: The study was carried out on human bladder carcinoma T24 cell line. Determination of cell viability was done using trypan blue exclusion method, apoptosis quantitative estimation – by DAPI staining and agarose gel electrophoresis for DNA fragmentation. Flow cytometry analysis, RT-PCR and Western blot analysis, colorimetric assay of caspase activity were applied as well.

RESULTS: It was found that in micromolar range of

concentrations beta-lapachone inhibited the viability of T24

cells by inducing apoptosis, which could be proved by

formation of apoptotic bodies and DNA fragmentation.

Treatment of T24 cells with beta-lapachone resulted in a

down-regulation of Bcl-2 expression and up-regulation of

Bax expression. beta-lapachone-induced apoptosis was also

associated with activation of caspase-3 and caspase-9,

inhibition of IAP expression, and degradation of poly

(ADP-ribose) polymerase, phospholipase C-gamma1 and

beta-catenin proteins. At the same time Fas and FasL levels

were inhibited upon treatment with beta-lapachone in a

concentration-dependent manner. Conclusion:

beta-lapachone-induced apoptosis in T24 cells is mediated,

at least in part, by the mitochondrial-signaling p

“It is an established fact that cancer cells grow

uncontrollably and are not programmed for cellular death

“apoptosis”.  Studies have been done that show that an

ingredient in Taheebo called beta-Lapachone induces

growth inhibition and programmed cellular death in

bladder cancer cells.”  For further information see:

National Center for Biotechnology Information

Cancer therapy with beta-lapachone. source PubMed

Pardee AB, Li YZ, Li CJ.

Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA

02115, USA. pardee@mbcrr.harvard.edu

Abstract

Beta-lapachone is an ortho naphthoquinone, originally

isolated from a tree whose extract has been used medicinally

for centuries. Recent investigations suggest its potential

application against numerous diseases. Its lethality at

micromolar (m) concentrations against a variety of cancer

cells in culture indicates its potential against tumor growth.

A few experiments with positive results have been performed that apply the compound to tumors growing in

animals.

Particularly promising is the remarkably powerful

synergistic lethality between beta-lapachone and taxol

against several

tumor cell lines implanted into mice; the mice did not

appear to be adversely affected. Enhanced lethality of

X-rays and

alkylating agents to tumor cells in culture was reported

when beta-lapachone was applied during the recovery

period,

because of inhibition of DNA lesion repair. Clinical trials are

still to be initiated. The detailed mechanism of cell death

induced by beta-lapachone remains for investigation. DNA

topoisomerase I was the first biochemical target of

beta-lapachone to be discovered, although its role in cell

death is not clear. A proposed mechanism of cell death is via

activation of a futile cycling of the drug by the cytoplasmic

two-electron reductase NAD(P) H: quinone oxidoreductase,

also known as NQO1, DT-diaphorase and Xip3. Death of

NQO1 expressing cells is prevented by the NQO1 inhibitor

dicoumarol, and cells with low NQO1 are resistant. At higher

drug concentrations the production of reactive oxygen

species (ROS)

appears to be responsible. Furthermore, this process is p53-

and caspase- independent. Either apoptotic or necrotic cell

death can result, as reported in various studies performed

under differing conditions. Beta-lapachone is one of a few

novel anticancer drugs currently under active investigation,

and it shows promise for chemotherapy alone and especially

in combinations.

Seterusnya sila baca dari sini

Sung Ok Kim¹, Jae Im Kwon², Dong-Eun Kim¹, Soo-Wan Nam¹, Won-Kyung Choe³ and Yung Hyun Choi^{2 1} Biomaterial Control(BK21 program), Dongeui University Graduate School, 995 Eomgwangno, Busanjin-gu, Busan, 614-714, Korea, Republic of, ² Biochemistry, Dongeui University College of Oriental Medicine, 45-1, Yungjung-2-dong, Busanjin-gu, Busan, 614-052, Korea, Republic of, ³ Food & Nutrition, Gimcheon College, 754, Samlack-dong, Gimcheon-si, Gyeongsanbuk-do, 740-704, Korea, Republic of

ABSTRACT

ß-lapachone, a quinone is a compound obtained from the bark of the lapacho tree (Tabebuia

avellanedae), was reported to have anti-inflammatory and anti-cancer activities. In this study, we

investigated novel functions of ß-lapachone about anti-metastasis and anti-invasion using human

hepatocarcinoma cell lines, HepG2 and HepG3. ß-lapachone dose-dependently inhibited cell

viability and migration of both HepG2 and Hep3B cells according to MTT assay and wound healing

assay. RT-PCR and Western blot data revealed that ß-lapachone dramatically induced the levels of

protein as well as mRNA expression of early growth response gene-1 (Egr-1) and throbospondin-1

(TSP-1) on early time and then decreased in a time-dependent manner. In addition, the

down-regulation of Snail and up-regulation of E-cadherin expression were observed in

ß-lapachone-treated HepG2 and Hep3B cells, which was associated with the decreased invasive

ability as measured by matrigel invasion assay. Taken together, our results strongly suggest that

ß-lapachone may be expected to inhibit progression and metastasis of hepatoma cells, at least in

part, by inhibiting the invasive ability of the cells via up-regulation of the expression of the Egr-1,

TSP-1 and E-cadherin.

Baca lapuran dari

Dana-Farbe Cancer Institute, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.