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cancer > cancer study 5
Cancer Study #5
Title
Anti-Tumor
Effects of Natural Products Maharishi Amrit Kalash-4
(MAK-4) and Maharishi Amrit Kalash-5 (MAK-5) on Cell
Transformation In Vitro and in Liver Carcinogenesis
in Mice.
Presented
at
Nineteenth Annual Convention of Indian Association for
Cancer Research and Symposium on Cancer Biology, Amala
Cancer Hospital and Research Center, Thrissur, India,
January 21-23, 2000.
Authors
F. Ferrari,* W.L. Hsiao,** G. Gerardi,* M. Statuto,Ú
G. Mazzoleni,‡ M. Marra,§ H. Sharma,¶ and D. Di Lorenzo.*
Conducted
at
**Laboratory of Biotechnology, Civic Hospital of Brescia,
25123 Brescia, Italy
**Department of Biology, The Hong Kong University of
Science and Technology, Hong Kong, China
Ú Institute of General Pathology, School of Medicine,
University of Milan, 20100 Milan, Italy
‡ Unit of General Pathology and Immunology, School
of Medicine, University of Brescia, 25123 Brescia, Italy
§ Center of Cytology, Gerontological Research Department
of I.N.R.C.A., 60121 Ancona, Italy
¶ Department of Pathology, College of Medicine
and Public Health, The Ohio State University, Columbus,
OH 43210 USA
Summary
Background: Maharishi Amrit Kalash-4 (MAK-4) and Maharishi
Amrit Kalash-5 (MAK-5) are herbal mixtures with anticancer
and anticarcinogenic properties. This investigation
evaluated the cancer-inhibiting effects of MAK-4 and
MAK-5 in vitro and in vivo. Methods: Aqueous extracts
of MAK-4 and MAK-5 were tested for effects on ras-induced
cell transformation in the Rat 6 cell line assessed
by focus formation assay. Urethane-treated mice were
put on a standard pellet diet or a diet supplemented
with MAK-4 and MAK-5. At 36 weeks, livers were examined
for tumors, sera for oxygen radical absorbance capacity
(ORAC), and liver homogenates for enzyme activities
of glutathione peroxidase (GPX), glutathione-S-transferase
(GST), and NAD(P)H: quinone reductase (QR). Liver fragments
of MAK-fed mice were analyzed for connexin (cx) protein
expression. Results: MAK-5 and a combination of MAK-5
plus MAK-4, inhibited ras-induced cell transformation.
There was a 46% reduction in the number of mice that
developed liver nodules when fed with MAK. MAK-treated
mice had a significantly higher ORAC (two-sided p<0.05)
compared to controls (200.2 + 33.7 vs. 152.2 + 15.7
ORAC units, respectively). MAK-treated mice had significantly
higher activities of GPX, GST, and QR compared to controls
(two-sided P<0.05, p<0.01, and p<0.01, respectively).
Livers of MAK-treated mice showed a time-dependent increased
expression of cx32. Conclusions: A MAK-supplemented
diet inhibits liver carcinogenesis in urethane-treated
mice. Possible mechanisms involving inhibition of oxidative
damage and up-regulation of connexin expression are
discussed.
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