Scientific Basis for Ayurvedic Therapies -21

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

Local treatments mentioned in Ayurveda, like medicated poultice (upanaha), sudation

(swedana), application of medicated pastes (lepana), and bloodletting (raktamokshana), are

being practiced by Ayurvedic physicians in cancer as well as various other disorders.

However, there is a lack of in vitro or in vivo trials and scientific studies to support their

role in different types of cancer.

16.9.4 Surgical Management

16.9.4.1 Indications

If a tumor (arbuda) does not resolve or respond to proper medical treatment, it should be

treated surgically. The main surgical treatments of tumors are excision (chhedana) and

excision with scrapping (lekhana).

Sushruta has described certain principles of the excision of tumors as follows:

1. Tumor mass is removed completely. The incomplete removal leads to recurrence

and poor prognosis.

2. Efforts are made to prevent the intraoperative spread of the tumor to distal organs.

Historically, application of metal tourniquets made up of iron, copper, zinc, and

lead were used around the tumor to control the spread. The mass is then destroyed

by cautery (agni), caustics (kshara), or surgically depending upon the depth and

extent of the tumor.

3. Sushruta advocated a minimal invasive technique in inoperable tumors or tumors

situated over vital areas (marma). In this case, a strong caustic thread (ksharasutra)

is passed across the center of its base with the help of a needle. The ends of the

thread should be tied firmly on either side, leading to avascular necrosis of the

tumor mass.

These principles of treatment occupy an important place in surgical oncology even today.

Application of tourniquets, the no-touch technique of excision, and the ligation of feeding

vessels are some of the important operative techniques that are still in practice to prevent

the spread of the tumor.

After surgical excision, the area is cauterized (agni/kshara) to achieve a complete cure.

Cleansing (shodhana karma) of the wound should be undertaken after excision of the tumor.

The wound has to be cleaned using the decoction of aparajita (Clitorea teratea), jati (Jasminum

grandiflorum), and karaveera (Neium odorum). The oil prepared from bharangi (Clerodendrum

serratum), vidanga (Embelia ribes), and the paste of triphala (Terminalia chebula, Terminalia

belerica, Emblica officinalis) can enhance the healing of wounds. Suppurated wounds may

be treated according to measures mentioned for the management of infected ulcers (dushta

vrana).

The efficacy of the above-mentioned drugs in wound healing has been established by

various experimental and clinical trials. Therefore, these drugs can be used safely in

conjugation with conventional surgical treatment.

16.9.4.2 Conventional Medicine

There are three sets of goals in conventional management of cancer patients: therapeutic,

human, and scientific.1 Ayurvedic medicine has similar goals. The therapeutic goal is to

cure patients and return them to normal life. If this is not attainable, then the next step in

this goal is to help patients achieve long, qualitatively satisfactory remission, or on a

tertiary level, a remission of any kind and finally terminal comfort care. The human goal

in oncology is that the needs of the patient, family, and social environment be understood

and met. The scientific goal requires special methods in oncology provided by specialists

to deliver optimal clinical care.

In conventional medicine, effective anticancer therapy has integrated medical management

with surgery and radiation therapy. The development of new cytotoxic and endocrine

agents and the introduction of biologic therapy based on recombinant synthesis of

interferon and cytokines have helped expand medical management. Not all patients are

candidates for cancer therapy because of limitations in available drugs or comorbidity

from other medical problems. In addition, not all tumors are responsive to chemotherapy

(Table 16.8). Although many of the tumors are manageable by various chemotherapeutic

15

Antitumor drugs fail to cure cancer because they cannot kill 100% of the cancer cells.

Even if one cell survives the chemotherapy, that cell can grow very quickly into millions

of cells. The result is a relapse of cancer because the body immunity defense does not

recognize the remaining cancer cells as foreign cells and thus does not kill them. Cancer

cells can hide behind the blood barriers for drugs, such as for blood-brain barrier, and

therefore do not get killed. The other mechanisms responsible for the failure of chemotherapy

are the metabolism of drugs to inactive form, removal of drugs by binding to

plasma proteins, rapid urinary excretion, and the development of resistance in the tumor

cells due to an increase in certain critical enzymes that are inhibited by the drug. For

example, tumors resistant to methotrexate were found to have high levels of dihydrofolate

reductase, a key enzyme.16–22 Transport across the cell membrane is also an obstacle in

reaching the agent to the malignant cell. This can sometimes present a formidable barrier

TABLE 16.8

Tumor Response to Chemotherapy in Conventional Medicine

Cure (>30%) of

Advanced Disease

Significant Cures

(5–30%)

Probably Increases

Survival

Adjuvant Treatment

Leading to

Increased Cure

Choriocarcinoma, acute

lymphocytic leukemia

(childhood), malignant

lymphoma (Hodgkin's

disease)

Hairy-cell leukemia

Testicular cancer

Childhood tumors (e.g.,

embryonal

rhabdomyosarcoma, Ewing’s

sarcoma, Wilm’s tumor)

Acute myelocytic leukemia

Acute lymphocytic leukemia

(adult)

Prtomyelocytic leukemia

Ovarian cancer

Bladder cancer

Small-cell lung cancer

Gastric cancer

Breast cancer

Multiple myeloma

Head and neck cancer

Breast cancer

Colon cancer

Osteogenic sarcoma

Early stage of large-cell

lymphoma

Source: From Goldman, L. and Bennett, J.C., Cecil Text Book of Medicine, Part XIV, W.B. Saunders, Philadelphia,

2000. With permission.

agents, they are associated with the causation of various toxicities (Table 16.9).

and may be one of the reasons why some tumors are insensitive to some of the chemotherapeutic

agents.23 Mechanisms of resistance to some common drugs are listed below.1

Cancer chemotherapy research in conventional medicine is primarily focused on developing

analogs of purines, pyrimidines, and various vitamins like folic acid, plant products,

and biological products. Various approaches have also been tried to overcome tumor

resistance to various drugs. For example, an attempt has been made to take advantage of

an increase in the enzyme responsible for the drug resistance. This approach is called

enzyme dependent lethal synthesis. It was speculated that tetrahydrohomofolic acid, an

analog of natural tetrahydrofolic acid (an inhibitor of thymidylate sythetase), may inhibit

DNA synthesis and overcome the resistance. Studies have shown that dihydrohomofolic

acid, a good substrate of dihydrofolate reductase, produced selective tumor inhibition

only in methotrexate-resistant tumors containing high levels of dihydrofolate reductase

enzyme.16–22 After administering dihydrohomofolic acid to tumor-bearing mice, several

folds of higher levels of tetrahydrohomofolic acid were found only in resistant tumors

containing high levels of dihydrofolate reductase enzyme than in the methotrexate sensitive

tumors confirming the hypothesis. A similar approach can be used with other agents

where an increase in a key enzyme is responsible for the drug resistance.

TABLE 16.9

Toxicity of Antitumor Drugs of Conventional Medicine

Type of Agent Major Clinical Toxicities

Alylating agents Cardiac, renal, hepatic, lungs, bone marrow, GI tract

Antifolates Bone marrow depression, intestinal epithelium, interstitial pneumonitis,

neurotoxicity

Pyrimidine analogs GI toxicity, ulceration of GI mucosa, neurotoxicity, cardiotoxicity,

myelosuppression, leucopenia

Purine analogs Bone marrow suppression, GI tract toxicity, hepatic necrosis,

immunosuppression

Vinca alkaloids Leukopenia, neurotoxicity, GI tract toxicity

Paclitaxel Neutropenia, bone marrow suppression, neurotoxicity, hypersensitivity

reactions

Actinomycin D GI tract toxicity, bone marrow suppression, hematopoetic suppression,

ulceration of oral mucosa

Daunorubicin, doxorubicin,

and idarubicin

Bone marrow suppression, GI tract toxicity, cardiac toxicity

Bleomycin Myelosuppression, cutaneouss toxicity, pulmonary toxicity, hyperthermia,

hypotension, exacerbations of rheumatoid arthritis

Plicamycin Bone marrow depression, liver and kidney toxicity, GI tract toxicity and

neurotoxicity

Platinum compounds Nephrotoxicity, hearing loss, peripheral neuropathy, myelosuppression,

hemolytic anemia, cardiotoxicity

Source: From Calabresi, P. and Chabner, B.A., Goodman & Gillman’s The Pharacological Basis of Therapeutics, Sec.

10, McGraw-Hill, New York, 1996. With permission.

Methotrexate Impaired transport or amplification of dihydrofolate

reductase

Cytarabine Decrease in deoxycytidine kinase or increase in cytidine

deaminase

5-Fluorouracil Increase in thymidylate synthetase enzyme

Cisplatin Decreased uptake, increase in repair enzymes

Taxol-Vinca alkaloids Multidrug resistance (MDR) expression, mutations in tubulin

(decreased binding)

Doxorubicin MDR expression, decrease or alterations in topoisomerase II

Irinotecan, topotecan Decrease in topoisomerase I

16.10 Scientific Basis

Giving due importance to the various drugs and formulations that have been mentioned

for the management of various arbuda, the modern-day researchers have been trying these

drugs in various animal models. The researchers’ goal is to find the drug’s mode of action,

realizing the dream of generating a magical potion for the eradication of cancers.

Various herbs used in Ayurveda are being researched both experimentally and clinically

in various institutions. Drugs and drug fractions with antitumor activity are summarized

presented below.

16.10.1 Clinical Studies

There are only two clinical studies available on antitumor herbal formulations. In the first

study,24 an Ayuravedic formula containing bhallataka (Semicarpus anacardium), rohitaka

(Amoora rohitaka), and yastimadhu (Glyceriza glabra) was studied on 100 patients with

different types of malignancy, as an adjuvant therapy, in a dose of 1.5 g/day in two divided

doses, given after food. The study concluded that this compound is effective in cancer

patients as evidenced by increases in body weight, appetite status, and hemoglobin percentage.

It also reduced the mortality rate in studied cases. It can be used along with

conventional therapy to improve the general condition of the patient. This compound can

be used in lymphoma patients along with chemotherapy and radiotherapy, as it reduces

the lymphophenic effect of chemotherapy and improves the hemoglobin level of the

patients.25

In the second study,26 the efficacy and side effects of an Ayurvedic arsenic-compound

formula were evaluated. This is in light of the fact that just over 100 years ago arsenic

was recognized in the West as useful in the control of blood counts in patients with chronic

myeloid leukemia.

16.10.2 In Vitro studies

In one in vitro study,27 extracts of the flowers of Calotropis procera (asclepiadaceae) and the

nuts of Semecarpus anacardium (anacardiaceae) displayed the strongest cytotoxic effect with

50% inhibitory dose (ID50) values of 1.4 and 1.6 mg/ml, respectively.

16.10.3 Animal Studies

16.10.3.1 Ashwagandha (Withania somnifera)

Withaferin A, isolated from the roots of W. somnifera, was found effective in Ehrlich ascitis

carcinoma when given at a dose of 30 mg/kg along with radiation therapy.28,29 Antioxidant

and detoxifying properties of W. somnifera may be responsible for chemopreventive activity.

30

Administration of 75% methanolic extract of W. somnifera was found to significantly

increase the total white blood cell (WBC) count in normal Balb/c mice and reduce the

leucopenia induced by a sublethal dose of gamma radiation. Treatment with W. somnifera

was found to significantly increase the bone marrow cellularity in mice. W. somnifera

in Table 16.10. Clinical, animal, and in vitro studies on some of the Ayurvedic herbs are

TABLE 16.10

Herbs and Herbal Fractions with Antitumor Activity

Plant

Botanical

Name

Parts

Used Dose Action as Mentioned in Classics Proven Actions Ref.

Bhallataka Semicarpus

anacardium

Fruit 3–6 g Lekhana (excises unhealthy tissues),

rasayana (rejuvenator)

Has antitumor activity against experimental mammary

carcinoma in animals

65,66

Ashwagandha Withania

somnifera

Root 3–6 g Shothahara (reduces swellings),

rasayana (rejuvenator)

Alcoholic extract of the root in doses of 400 mg/kg and

above produces complete regression of two-stage skin

carcinogenesis induced by DMBA and croton oil

35,67,68

Kumkuma Crocus sativa Stamens 1/2 –1 g Shothahara (reduces swellings),

rasayana (rejuvenator)

Has antitumor activity toward sarcoma-180 and Ehrlich

ascites carcinoma (EAC) solid tumors in mice

69

Bhunimba Andrographis

paniculata

All parts 1–3 g Raktashodhaka (purifies vitiated

blood), shothahara (reduces

swellings)

Prevents chemotoxicity including carcinogenicity 70

Tulasi Ocimum

sanctum

Leaf,

seed,

root

1–3 g Vishaghna (detoxifies), shothahara

(reduces swellings), raktashodhaka

(purifies vitiated blood)

Reduces 20-methylcholanthrene-induced tumor

incidence and tumor volume

71

Manduka parni Centella asiatica All parts Juice

10–20

ml

Kaphahara (cleanses vitiated kapha),

shothahara, (reduces swellings),

rasayana (rejuvenator)

Retards the development of solid and ascites tumors and

increases the life span of these tumor-bearing mice

72

Arka Calotropis

procera

Root,

latex,

flower

0.5–1 g Kaphashamaka (pacifies vitiated

kapha), shothahara (reduces

swellings), raktashodhaka (purifies

vitiated blood), vishaghna

(detoxifier)

Displays the strongest cytotoxic effect with ID50 values of

1.4 mg/ml

27

Chitraka Plumbago rosea Root

bark

1–2 g Lekhana (excises unhealthy tissue),

shothahara (reduces swellings),

rasayana (rejuvenator)

Used with radiation to enhance the tumor-killing effect 73

Bakuchi Psoralea

coryfolia

Seed,

seed oil

1–3 g Kaphagna (pacifies vitiated kapha),

shothahara (reduces swellings),

vrana shodhana (cleanses chronic

wounds), vrana ropana (heals

wounds)

100 mg/kg body weight (of the active fraction) inhibits

the growth and delays the onset of papilloma formation

in mice; the active fraction at the same dose, when

administered orally inhibits the growth of

subcutaneously injected 20-methylcholanthereneinduced

soft tissue fibrosarcoma significantly

74

Katuki Picrorhiza

kurroa

Root 1/2 –1 g Kaphagna (pacifies vitiated kapha),

shothahara (reduces swellings),

raktashodhaka (purifies vitiated

blood), lekhana (excises unhealthy

tissue)

Picroliv (100 and 200 mg/kg) inhibits the sarcoma

development by 47 and 53%; it also delays the onset of

first skin tumor in the group of animals treated with

Picroliv; Picroliv administration increases the life span

of transplanted Dalton’s lymphoma ascites (DLA) and

Ehrlich ascites carcinoma (EAC)-harboring mice and

reduces the volume of transplanted solid tumors

75

Aragvadha Cassia fistula Fruit

pulp,

root

bark

5–10 g Kaphashodhaka (pacifies vitiated

kapha), shothahara (reduces

swellings)

Increases life span by decreasing the tumor volume and

viable tumor cell count in the EAC tumor hosts;

improves the hematological factors after methanolic

extract treatment, like hemoglobin content, red blood

cell count and bone marrow cell count of the tumorbearing

mice

76

Kumari Aloe vera Leaf 10–20 ml Kaphahara (pacifies vitiated kapha),

shothahara (reduces swellings),

vrana ropana (heals wounds),

raktashodhaka (purifies vitiated

blood)

Detoxifies reactive metabolites including chemical

carcinogens and drugs

77

Kalajaji Nigella sativa Seed 1–3 g Kaphashamaka (pacifies vitiated

kapha), lekhana (excises unhealthy

tissue), shothahara (reduces

swellings)

In vivo EAC tumor development is completely inhibited

by the active principle at the dose of 2 mg/mouse/day

¥1016

78

Vamsha Bambusa

arundinacea

Root,

leaf,

Shoot

50–100

ml

Kaphashamaka (pacifies vitiated

kapha), lekhana (excises unhealthy

tissue), vishaghna (detoxifier)

Antitumor activity against benzopyrene and

4-nitroquinolince-1-oxide-induced tumors is highest

with 1% bamboo leaf extracts (0.71 mg/ml) and a direct

action of bamboo leaf extracts on tumor cells is indicated

79

Hingu Ferula narthex Latex Up to

0.5 g

Kaphahara (normalizes vitiated

kapha)

Asafoetida is a potent antioxidant and can afford

protection against free radical mediated diseases such as

carcinogenesis

80

Methika Trigonella

foenum-

Graecum

Seed 1–3 g Shothahara (reduces swellings) Has an anti-inflammatory and antineoplastic effect 81

Amala Emblica

officinalis

Gaertn

Fruit 4–10 g Shothahara (reduces swellings) Antioxidant, antitumor, chemopreventive, prostate

cancer, immunomodulator, anticlastogenic radiation

protection

82–96

© 2004 by CRC Press LLC

298 Scientific Basis for Ayurvedic Therapies

treatment of irradiated mice normalized the ratio of normochromatic erythrocytes and

polychromatic erythrocytes. Major activity of W. somnifera seems to be in the stimulation

of stem cell proliferation.31

The alcoholic extract of dried roots of W. somnifera and Withaferin A showed significant

antitumor and radio-sensitizing effects in experimental tumors in vivo without any noticeable

systemic toxicity. The mechanism of action, however, is not clear. The studies indicate

that W. somnifera could prove to be a good natural source of a potent and relatively safe

radio-sensitizer and chemotherapeutic agent. Further studies are needed to explore the

clinical potential of the plant for cancer therapy.32

W. somnifera was injected at a dose of 500 mg/kg to tumor-bearing mice (tumor size: 50

± 5 mm3) for 10 days with one local exposure of radiation therapy followed by hyperthermia.

It significantly increased the tumor cure rate, produced a delay in the growth of

partially responding tumors, and increased animal survival. Study concluded that W.

somnifera, in addition to having a tumor-inhibitory effect, also acts as a radio sensitizer.33

W. somnifera extract also inhibited 20-methylcholanthrene-induced sarcoma development

in mice at a dose of 20 mg/day.34 W. somnifera extract was also found to reduce two-stage

skin carcinogenesis induced by DMBA and croton oil.35

Withaferin A reduced survival of V79 cells in a dose-dependent manner. LD50 for

survival was 16 mM. One-hour treatment with a non-toxic dose of 2.1 mM before irradiation

significantly enhanced cell killing, giving a sensitizer enhancement ratio (SER) of 1.5 for

37% survival and 1.4 for 10% survival.36 W. somnifera was found to significantly reduce

leucopenia induced by cyclophosphamide (CTX) treatment. The total WBC count on the

12th day of the CTX-treated group was 3720 cells/mm3; the WBC count in CTX-treated

animals that were simultaneously treated with WS was 6120 cells/mm3. Withania extract

increased the number of alpha-esterase positive cells (1130/4000 cells) in the bone marrow

of CTX plus W. somnifera-treated animals, compared with the CTX-treated group (687/

4000 cells).37

W. somnifera was also found to enhance the levels of interferon gamma (IFN-gamma)

(75.87 pg/ml), Interleukin-2 (IL-2) (14.16 pg/ml), and granulocyte macrophage colonystimulating

factor (GM-CSF) (49.22 pg/ml) in normal Balb/c mice. The lowered levels of

IFN-gamma (30 pg/ml), IL-2 (4.5 pg/ml), and GM-CSF (19.12 pg/ml) after treatment with

CTX was reversed by the administration of W. somnifera extract (IFN gamma = 74 pg/ml;

IL-2 7.5 = pg/ml; GM-CSF = 35.47 pg/ml). W. somnifera extract lowered the levels of tumor

necrosis factor alpha (TNF alpha) production. Administration of bone marrow cells from

donor mice treated with WS extract increased the spleen nodular colonies in irradiated

mice (8.33) compared with those treated with normal bonemarrow cells (3.03). The number

of nodular colonies increased significantly after continuous treatment with WS. These

results indicate the immunopotentiating and myeloprotective effects of W. somnifera.38

W. somnifera extract was also found effective as a chemopreventive agent. W. somnifera

protected against 20-methylcholanthrene-induced fibrosarcoma tumors in Swiss albino

mice. A single subcutaneous injection of 200 mg of 20-methylcholanthrene in 0.1 ml of

dimethylsulphoxide into the thigh region of mice produced a high incidence (96%) of

tumors. Oral treatment of animals with 400 mg/kg body weight of W. somnifera extract

(1 week before injecting 20-methylcholanthrene and continuing until 15 weeks thereafter)

significantly reduced the tumor incidence and tumor volume and enhanced the

survival of the mice, compared with the untreated 20-methylcholanthrene-injected mice.

The occurrence of tumors was also delayed in the treatment group. Liver biochemical

parameters revealed a significant modulation of reduced glutathione, lipid peroxides,

glutathione-S-transferase, catalase, and superoxide dismutase in extract-treated mice

compared with 20-methylcholanthrene-injected mice. The authors suggested that the

mechanism of chemopreventive activity of Withania somnifera extract may be due to its

antioxidant and detoxifying properties.39 W. somnifera was also found to increase the

neutrophil count in mice with paclitaxel-induced neutropenia.40

16.10.3.2 Aloe vera Linn.

Di (2-ethylhexyl) phthalate (DEHP), an active principle isolated from Aloe vera Linn., has

been shown to have antileukemic and antimutagenic effects in vitro in Salmonella typhimurium

TA98 and TA 100 strains.41 Aloes potentiated the antitumor effect of 5-fluorouracil

and cyclophosphamide as components of combination chemotherapy.42 Aloe-emodin, a

hydroxyanthraquinone present in Aloe vera leaves, has been shown to have a specific in

vitro and in vivo antineuroectodermal tumor activity.43

Aloe vera has been claimed to contain several important therapeutic properties, including

anticancerous effects. The effect of this drug was studied on a pleural tumor in rat (Yoshida

AH-130, ascite hematoma cells) and proved its therapeutic use in cancer.44

In one study, the antigenotoxic and chemopreventive effect of Aloe barbadensis Miller

(polysaccharide fraction) on benzo[a]pyrene (B[a]P)-DNA adducts was investigated in

vitro and in vivo. Aloe showed a time-course and dose-dependent inhibition of [3H]B[a]PDNA

adduct formation in primary rat hepatocytes (1 ¥ 106 cells/ml) treated with [3H]B[a]P

(4 nmol/ml).45 The growth of human neuroectodermal tumors is inhibited in mice with

severe combined immunodeficiency without any appreciable toxic effects on the animals.

The compound does not inhibit the proliferation of normal fibroblasts nor that of hemopoietic

progenitor cells. The cytotoxicity mechanism consists of the induction of apoptosis,

whereas the selectivity against neuroectodermal tumor cells appear to depend upon a

specific energy-dependent pathway of drug incorporation.46

Crude modified aloe polysaccharide (MAP) activated macrophage cells and stimulated

fibroblast growth. Under the same conditions, native Aloe barbadensis gel had no effect on

macrophage activation. MAP prevented ultraviolet B (UVB) irradiation-induced immune

suppression as determined by contact hypersensitivity (CHS) response in C3H/HeN

mice.47 Aloin- or sennoside-enriched diets (0.03%) did not promote incidence and growth

of adenomas and carcinomas after 20 weeks in a model of dimethylhydrazine-induced

colorectal tumors in male mice. In addition, no significant changes in serum electrolytes

and parameters of hepato- and nephrotoxicity were observed in the aloe-fed mice.47

A new immunostimulatory polysaccharide called Aloeride from commercial Aloe vera

(Aloe barbadensis) juice has been isolated and characterized. It is between 4 and 7 million

Da, and its glycosyl components include glucose (37.2%), galactose (23.9%), mannose

(19.5%), and arabinose (10.3%). Although Aloeride comprises only 0.015% of the aloe juice

dry weight, its potency for macrophage activation accounts fully for the activity of the

crude juice.48

16.10.3.3 Coleus forskohlii

Forskolin, a diterpene from C. forskohlii, is a potent platelet aggregation inhibitor. It has

been found to strongly inhibit the melanoma cell-induced human platelet aggregation and

tumor colonization. The study suggests that forskolin could prove to be valuable in the

clinic for the prevention of cancer metastasis.49

Roidex, a formulation of squalene, vitamin E, and Aloe vera, produced chemopreventive

effect in chemically induced skin tumors in CD-1 mice. The tumors were induced by 7,12-

dimethylbenz[a]-anthracene (DMBA) and promoted with 12-O-tetradecanoylphorbol-13-

acetate (TPA). The mice were treated with either mineral oil, 5% squalene, or Roidex. There

was a regression of 33.34% of the tumors in the Roidex-treated group (39 to 26 tumors)

compared with the nontreated group, whose tumors regressed only 3.44% (29 to 28

tumors).50 An immunomodulator fraction extracted from Aloe vahombe (Alva) was found

to protect mice against bacterial, parasitic, and fungal infections. It also produced cures

only in the case of the McC3-1 tumor; under different experimental conditions, the growth

rate of tumors in animals treated was found to be slower than in those untreated.51

16.10.3.4 Andrographis paniculata Nees

The methanol extract of the aerial part of Andrographis paniculata Nees showed potent cell

differentiation-inducing activity on mouse myeloid leukemia (M1) cells.52

16.10.3.5 Santalum album

The essential oil, emulsion, or paste of S. album has been used in India as an Ayurvedic

medicinal agent for the treatment of inflammatory and eruptive skin diseases. Sandlewood-

oil treatment showed chemopreventive effect in DMBA-initiated and TPA-promoted

skin papillomas tumor model and TPA-induced ornithine decarboxylase (ODC)

activity in CD-1 mice. Sandalwood-oil treatment significantly decreased papilloma incidence

by 67%, multiplicity by 96%, and TPA-induced ODC activity by 70%. The study

suggests that the oil could be an effective chemopreventive agent against skin cancers.53

16.10.3.6 Picrorrhiza kurroa

P. kurroa extract has been shown to have antitumor and anticarcinogenic activity in 20-

methylcholanthrene (20 MC)-induced tumor model after oral administration. The extract

also inhibited transplantable tumors.54

16.10.3.7 Cystone

Cystone, a polyherbal ayurvedic preparation, was found to protect tumor-bearing mice

from cisplatin-induced nephrotoxicity when given intraperitoneal 1 h before cisplatin.

Pretreatment with cystone did not reduce the antitumor activity of cisplatin. The study

shows potential for use in protecting patients from nephrotoxicity of cisplatin.55

16.10.3.8 Sesame Oil

Sesame oil is extensively used as topical application in Ayurveda for skin health. In one

study, it was found that sesame and safflower oils, both of which contain large amounts

of linoleate in triglyceride form, selectively inhibited malignant melanoma growth over

normal melanocytes; coconut, olive, and mineral oils, which contain little or no linoleate

as triglyceride, did not. Further studies showed that only linoleic acid was selectively

inhibitory, whereas palmitic and oleic acid were not. These fatty acids were tested in the

range of 3 to 100 mg/ml. The study suggests that certain vegetable oils rich in linoleic

acid, such as the sesame oil, recommended for topical use by Ayurveda, may actually

contain selective antineoplastic properties.56

16.10.3.9 Terminalia arjuna

Methanol extract of T. arjuna was found to inhibit the growth of human normal fibroblasts

(WI-38) in vitro without any effect on normal cells. A cyclin-dependent kinase inhibitor,

p21WAF1, was induced in the transformed cell by T. arjuna. It is likely that T. arjuna has

components that can inhibit of transformed cell by p53-dependent and independent

pathways.57

16.11 Conclusions and Future Research

It is evident that early Ayurvedic physicians had a good understanding of etiology, clinical

manifestations, symptoms, classification, malignant and benign nature of tumors, metastasis,

recurrence diagnosis, prognosis, and treatment. It is remarkable that the basic information

is fairly consistent with the current knowledge in these areas given the technology

available 500 years ago. The physicians also recognized the fact that malignant tumors

must be completely and extensively excised so that not a trace of tumor is left in the body

for even a trace can grow back to a tumor. This is also consistent with the current

knowledge about the nature of malignant tumors and their treatment. Various treatment

methods, both local and systemic, and various herbal formulations found useful in many

tumors are presented. The review has shown that Ayurvedic therapies are useful as an

adjuvant to conventional chemotherapy. The following areas are identified for further

research: (1) the use as an adjuvant to improve the well-being of the patient, (2) protection

against the drug cytotoxicity (the major dose limiting side effect), (3) chemoprevention to

reduce the cancer incidence, and (4) immunomodulation to help the body respond better

to cancer chemotherapy.

References

1. Goldman, L. and Bennett, J.C., Eds., Oncology, in Cecil Text Book of Medicine, Part XIV, W.B.

Saunders, Philadelphia, 2000.

2. Mishra, L.C., Criteria for Classifying Carcinogens in Consumer Products for Purpose of Labeling

under the Federal Hazardous Substances Act. Labeling Requirements for Art Materials

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Om Tat Sat

                                                        

(Continued...) 

(My humble salutations to H H Maharshi ji,  Brahmasri Sreeman Lakshmi Chandra Mishra ji and other eminent medical scholars and doctors   for the collection)