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Moringa oleifera Lamarack (Moringaceae)


Moringa pterygosperma Gaertn.

Vernacular Names:

Malaysia: Kelor

Horseradish-tree, Drumstick-tree


Saijan [1]

Sanskrit: Shigru [1]

General Information


A pan-tropical species that belongs to a monogenic family of shrubs and trees, Moringaceae.  It is full in leaf at the end of the dry season and found in many countries in the tropics and subtropical regions. It is a native to sub-Himalayan tracks of India, Pakistan, Bangladesh and Afghanistan. A native tree of northern India, is now widely cultivated throughout the tropics and is found in many countries of Africa, Asia and South America regions.  All parts of the M. oliefera tree are edible and have long been consumed by humans. [1]

Plant Part Used

All parts. Leaves, roots, seeds, barks, fruits, flowers, immature pods. [2]

Chemical Constituents

Zeatin, quercetin, b-sitosterol, caffeoylquinic acid and kaempferol. It has high nutritional value and is a good source of protein, vitamins, b-carotene, amino acids and various phenolics. [2] M. oleifera leaves contain large amounts of calcium (19.3-22.4 mg/g dry weight) and significant amounts of selenium (27.1 µg/ g dry weight) and phosphorus (2.5-6.3 mg/g dry weight). [3],[4] The leaves also contained 17.1 mg total protein/mg dry weight.  The various essential amino acids were present in comparable proportions to the World Health Organization (WHO) egg white-based, protein standard. M. oleifera leaves contain relatively large amounts of α-linolenate (12.3 mg/g) but less than 1.0 mg/g of linoleate. [3]

The ethanol extract of M. oleifera seeds contained O-ethyl-4-(a-L-rhamnosyloxy)benzyl carbamate, 4(a-L-rhamnosyloxy)-benzyl isothiocyanate, niazimicin, niazirin, b-sitosterol, glycerol-1-(9-octadecanoate), 3-O-(6'-O-oleoyl-b-D-glucopyranosyl)-b-sitosterol, and b-sitosterol-3-O-beta-D-glucopyranoside. [5]

The leaves contained 90 mg/kg a-tocopherol [6] and total carotene (1.93 mg/g dry weight), b-carotene (0.93 mg/g dry weight), ascorbic acid (6.6 mg/g dry weight ), total iron (0.26 mg/g dry weight ) and oxalic acid (11.2 mg/g dry weight).  The leaves retained 50% of their content of b-carotene with shade dehydration. [4] Other antioxidants present include a- and g-tocopherol, vitamin A and phenolic compounds such as quercetin and kaempferol, flavonoids, anthocyanins. [1] The leaves also contain nitrile glycosides, viz. niaririn and niazinin and mustard oil glycosides, niaziminin A and niaziminin B. [7]

The fruits contain proteins, fats, carbohydrates, minerals, fibre, vitamin A, b-nicotinic acid, ascorbic acid, tocopherol, oestrogenic substances and b-sitosterol. [8]

The root-bark contains the alkaloid moringine and moringinine, and an antibiotic principle, pterygospermin. [7]

Traditional Use:

A traditional herb used M. oleifera throughout Southeast Asia and Indo-China. Every part of this plant is valued for food and it is used for stimulation of digestion and treating septicemia, as a remedy for venereal diseases and diseases of the chest, as a stimulant, antipyretic, tonic and for treatment of convulsions. [9]

The flowers, leaves, and roots are used in folk remedies for tumors while the seed for abdominal tumors. [1],[10] The root decoction is used in Nicaragua for dropsy.  Root juice is applied externally as rubefacient or counter-irritant. Leaves applied as poultice to sores, rubbed on the temples for headaches, and said to have purgative properties. Bark, leaves and roots are acrid and pungent, and are taken to promote digestion. Oil is somewhat dangerous if taken internally, but is applied externally for skin diseases. The leaves are also used by Indians as a hypocholesterolemic agent in obese patients and patients with heart disease. [8],[10]

The bark regarded as antiscorbic, and exudes a reddish gum with properties of tragacanth; sometimes used for diarrhea.  The roots are bitter, act as a tonic to the body and lungs, used as an emmenagogue, expectorant, mild diuretic and used for epilepsy and hysteria.

The uses of the M. oleifera roots were described in Indian Materia Medica for the treatment of ailments which include asthma, gout, lumbago, rheumatism, enlarged spleen or liver, internal deep seated inflammations and calculous affections which include kidney stones. [1],[7],[11] The leaf, flower, fruit and bark are used in herbal medicines for paralysis and hypertension, for the treatment of ascites, rheumatism, venomous bites and for enhancing the cardiac function, maintenance of hematological, hepatic and renal functions while the leaves are useful for scurvy and catarrhal affections. [1],[11],[12]

The leaves are eaten as a vegetable in Nigeria and as food for infants and childrenin South India to prevent the development of vitamin A deficiency blindness. [10]

The flocculants in M. oleifera seeds are used to purify water.  The seed kernels can remove lead, iron and cadmium ions from contaminated water while the seed powder was used to remove cadmium from aqueous systems. [1]

Pre-Clinical Data


Antiurolithiasis activity


The aqueous and alcoholic extracts of M. oleifera root-wood (dose of each extract used was 200 mg/kg body weight) were tested for antiurolithiatic activity in hyperoxaluria model using male albino rats. [7] The hyperoxaluria was induced by adding ethylene glycol (0.75%) in the drinking water for induction of renal calculi till the 28th day. For determination of their curative effects, each of the extracts was given to hyperoxaluria rats beginning from the 15th to the 28th day while for determination of preventive effects, the extracts were given daily by the oral route form the 1st till the 28th day.  Cystone (750 mg/kg body weight), the reference antiurolithiatic drug, was given from day 15th till day 28th.

Both extracts significantly reduced the elevated levels of oxalate, calcium and phosphate in urine and kidney that were induced by ethylene glycol, in both the in curative and preventive regimens, as compared to cystone-treated animals.  Increased deposition of stone forming constituents (oxalate, phosphate, calcium) in the kidneys of calculogenic rats was also significantly lowered by the curative and preventive treatments using aqueous and alcoholic extracts. Both extracts given for curative or preventive purposes reduced the elevated levels of serum creatinine, uric acid and blood urea nitrogen, which were observed in calculi-induced animals.  The results indicate that the root-wood of M. oleifera is endowed with antiurolithiatic activity.  The mechanism is unknown but may involve increased diuresis and decreased urinary concentrations of stone-forming constituents. [7]


Antioxidant activity


The protective effects of M. oleifera was studied in antitubercular (TB) drug (isoniazid, rifampicin, and pyrazinamide)-induced toxicity in rats. The antiTB drugs increased hepatic marker enzymes and lipid peroxidation with concomitant decrease in the levels of vitamin C, reduced glutathione, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST).  M. oleifera and silymarin significantly lowered the antiTB-drug induced increase in hepatic marker enzymes and lipid peroxidation and simultaneously increased the levels of antioxidants. The protective effects of M. oleifera extract probably involve its ability to decrease liver lipid peroxides and to enhance the. [13]

Protection against arsenic-induced oxidative stress activity

M. oleifera seed powder (250 and 500 mg/kg, orally) given 1 h prior to arsenic (2.5 mg/kg, intraperitoneally for 6 weeks) in mice led to amelioration of arsenic-induced oxidative stress, reduced the arsenic body burden and may be of benefit during arsenic chelation therapy with a thiol chelator. [1] M. oleifera reversed the effects of arsenic by significantly increasing the activities of SOD, catalase, GPx and significantly elevated the levels of reduced glutathione (GSH) in the liver and kidney.  These parameters were depressed by arsenic.  Blood reactive oxygen species (ROS), liver metallothionein (MT) and lipid peroxidation levels were simulataneous decreased by about 57%, 64% and 17%, respectively.  Both doses of arsenic significantly protected the blood, liver and brain from reactive oxygen species while the higher dose of 500 mg/kg of M. oleifera seed powder produced greater protection in the kidney as compared to the lower dose.  The arsenic inhibited heme synthesis in the blood and liver as indicated by inhibited liver d-aminolevulinic acid dehydratase (ALAD) activity and this was accompanied by elevations in urinary excretion of aminolevulinic acid (ALA).  The higher, not the lower dose of M. oleifera seed powder reversed ALAD activity inhibition but both doses significantly decreased urinary ALA excretion in arsenic-exposed mice as compared to controls.  M. oleifera (particularly at 500 mg/kg dose) reversed the significant elevation in platelet counts that was elicited by arsenic and reversed arsenic-induced depletion in liver activities of SOD, catalase and GPx and arsenic-induced increase in thiobarbituric acid reactive substances (TBARS). In the kidney, M. oleifera (particularly at 500 mg/kg dose) provided significant recovery from arsenic-induced decrease in catalase activity and arsenic-induced increase in TBARS levels while in the brain, the seed powder protected against arsenic-induced depletion in brain SOD activity and arsenic-induced increase in TBARS levels. The increase in hepatic metallothionein induced by arsenic was lowered by M. oleifera which also markedly depleted arsenic concentrations in blood, liver and kidney without affecting arsenic concentrations in the brain.  The changes elicited by the 500 mg/kg dose were more pronounced than those elicited by the lower dose.

M. oleifera seed powder did not affect blood and tissue copper, zinc and iron concentrations in normal and arsenic-exposed animals.  The protection against arsenic-induced oxidative stress was attributed to the direct scavenging action of M. oleifera as the seeds contain high concentrations of sulfhydryl (-SH) containing amino acids, methionine and cysteine, which are capable of stimulating GSH synthesis besides providing additional binding sites for arsenic for its ultimate removal. [1]

Hypocholesterolemic activity


The crude aqueous leaf extract of M. oleifera possessed hypocholestrolaemic activity when given to rats fed a high fat diet which increased total cholesterol levels in the serum, liver and kidney. M. oleifera extract (in a daily dose of 1 mg/g body weight, p.o.) reduced the high-fat diet-induced increases in serum, liver and kidney cholesterol levels and increased the high-fat diet-induced decrease in serum albumin levels.  Both the high-fat diet and the extract in high-fat diet animals did not alter serum total proteins. [10]

Central inhibitory activity


M oleifera aqueous extract (350 mg/kg) potentiated pentobarbitone sleeping time, increase serum 5-hydroxytryptamine (5-HT) levels and alpha wave activity in adult albino rats.  The extract inhibited awareness, touch response, motor activity, righting reflex and grip strength.  The effects of the extract was thought to be mediated through 5-HT. [14]

M oleifera standardized aqueous root extract (100-450 mg/kg, p.o.) given chronically to penicillin-convulsed adult albino rats elicited central inhibitory activity. The pretreatment of the rats with M. oleifera aqueous extract led to inhibition of penicillin-induced seizure and a markedly reduced locomotor activity. 5-HT level was increased by M. oleifera while dopamine levels were decreased in the cerebral cortex, midbrain, caudate nucleus and cerebellum.  The norepinephrine level was only decreased in the cerebral cortex. [15]

Wound healing property activity

The aqueous extracts of M. oleifera (300 mg/kg body weight) showed significant wound healing properties in resutured incision, excision and dead space wound models in rats.  There were significant increases in the wound closure rate, skin-breaking strength, granuloma breaking strength, granuloma dry weight, the hydroxyproline content while the scar area was decreased. The prohealing effects of M. oleifera were attributed to increased collagen deposition and to better alignment and maturation. [16]

Radioprotective activity

The 50% methanolic extract of M. oleifera (150 mg/kg body weight, i.p.) given as a single dose or in 5 daily doses of 30 mg/kg body weight each, protected albino mice from the effects of whole body gamma irradiation (4 Gy) which was instituted after 1 hour treatment with the extract. Higher bone marrow protection was seen with the fractionated method of extract administration than its administration in a single dose.  The extract significantly reduced the percent of aberrant cells on day 1 which returned to normal levels by day 7 post-irradiation.  There was higher survival at 30 days post-irradaition.  In vitro, M. oleifera dose-dependently prevented the generation of free radical activity via the Fenton reaction. [17]

Antifungal activity

Extracts of M. oleifera were tested on pathogenic fungi using broth dilution and agar plate methods. M. oleifera (1:10 dilution) inhibited the growth of Basidiobolus haptosporus, B. ranarum, Trichophyton rubrum and T. mentagrophytes. [18]

The essential oil (crude and oxygenated sub-fraction) and seed extracts (ethyl acetate and butanol sub-fractions) showed anti-fungal activity against T. rubrum, T. mentagrophytes, E. floccosum and M. canis while the leaf crude extract and its sub-fractions had little effect on dermatophytes (11). The MICs of the essential oil and its sub-fraction ranged from 0.1 mg/mL (E. floccosum) to 1.6 mg/mL (T. rubrum)).  The ethyl acetate fraction of the seed extract and the oxygenated sub-fraction of the essential oil showed strong anti-fungal activity (MIC of 0.156 mg/mL and 0.2 mg/mL, respectively) against M. canis, a zoophilic dermatophyte which cause marked inflammatory reactions in humans especially in the beard area, hair, glabrous skin and hands.  Fungal cells treated with 70% EtOH crude extract of M. oleifera seeds for 24 hours experienced cytoplasmic membrane rupture and seriously damaged intracellular components although no leakage was seen.  The extracts of M. oleifera was postulated to interact with the lipid bilayers in fungal membranes leading to the separation of the outer and inner membranes with consequent influx of water, cell swelling, and cell death. [11]

Antitumour activity

The antitumour promoting activity of 4(a-L-rhamnosyloxy)-benzyl isothiocyanate, niazimicin, b-sitosterol-3-O-b-D-glucopyranoside and 3-O-(6'-O-oleoyl-b-D-glucopyranosyl)-b-sitosterol were determined in an in vitro assay which tested their inhibitory effects on Epstein-Barr virus-early antigen (EBV-EA) activation in Raji cells induced by the tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA).  All compounds inhibited EBV-EA activation although the first three compounds showed highly significant activity.  In vivo, niazimicin exhibited potent antitumor promoting activity in the two-stage carcinogenesis model in mouse skin using 7,12-dimethylbenz(a)anthracene (DMBA) as the initiator and TPA as the promoter. [5]

Niaziminin, a thiocarbamate, isolated from the leaves of M. oleifera inhibited the tumor promoter teleocidin B-4 induced EBV activation in Raji cells. The structure-activity relationships indicated an acetoxy group present at the 4'-position of niaziminin is important and indispensable for inhibition (19).  A naturally occurring isothiocyanate, 4-[(4'-O-acetyl-alpha-L-rhamnosyloxy)benzyl] isothiocyanate, also significantly inhibited activation of EBV indicating that the isothiocyano group is a critical structural factor for activity. [19]

The antiproliferative activity of M. oleifera extract was assayed in human cell lines, viz, erythroleukemia K562, B-lymphoid Raji, T-lymphoid Jurkat and erythroleukemia HEL cell lines.  The low concentrations of M. oleifera inhibit the interactions between nuclear factors and target DNA elements which mimic the sequences recognized by nuclear factor kappaB (NF-kappaB) as determined by the electrophoretic mobility shift assay.  The results point to the possibility of finding compounds in M. oleifera which may have anticancer and/or anti-inflammatory actions. [20]

The ethanolic extract of M. oleifera is a potential source of anticancer compounds as evidenced by its cytotoxicity (measured by the MTT assay) on HL-60, CEM, HCT-8 and B-16 tumor cell lines with LD50 values of 60.0, 12.7, 113.8 and 28.8 µg/mL, respectively.  The crude extract showed LD50 values of less than 30 µg/mL in two cancer cell lines, thus fulfilling the criteria of the American National Cancer Institute which stated a upper IC50 limit of 30 µg/mL for considering a crude extract to show promise for further purification for anticancer activity.  The extract also showed moderate inhibitory activity on sea urchin egg development with IC50 values at first cleavage, third cleavage and blastulae of the embryonic stage of 169.4, 119.5 and 52.5 µg/mL, respectively.  The cytotoxicity of M. oleifera ethanolic extract was not related to membrane disruption as it was found to be inactive in the mouse erythrocyte hemolytic assay with an EC50 value of more than 2500 µg/mL.  The extract was not active in the brine shrimp lethality assay. [21]

The hydro-alcoholic extract of M. oleifera (125 and 250 mg/ kg body weight given for 7 and 14 days, respectively) significantly increased the activities of hepatic cytochrome b5, cytochrome P-450, catalase, GPx, glutathione reductase (GR), acid soluble sulfhydryl content (-SH ) and a significant decrease in hepatic MDA levels when compared to controls.  The higher dose significantly increased GST activity.  The chemopreventive potential of the extract was determined in skin papillomagenesis studies.  Topical application of the extract (5 mg/kg body weight) in the peri-initiation phase i.e. 7 days before and 7 days after DMBA application, during the promotional phase i.e. starting application from the day of croton oil exposure and continued to the end of the study, and its application during both the peri and post initiation stages i.e. 7 days prior to DMBA application and continued to the end of the study, led to significant decreases in the percentage of mice with papillomas and a significant decrease in the average number of papillomas per mouse and as compared to controls.  The percentage inhibition of tumor multiplicity in the three groups above was found to 27%, 72%, and 81%, respectively. [22]

Regulation of hyperthyroidism activity

The aqueous extract of young, tender, healthy leaves of M. oleifera (175 mg kg/body wt./day, p.o. for 10 days) produced a significant increase in the serum T4 concentration with concomitant decreases in serum T3 concentration and T3:T4 ratio in female, not in male rats. M. oleifera (175 mg kg/body wt.) also reduced lipid peroxidation in the liver but did not change hepatic SOD and catalase activities.  Since significant effects of M. oleifera on thyroidal hormone status were elicited in female rats, the experiment was repeated with a higher dose of the aqueous M. oleifera extract (350 mg/kg/ body wt./day, p.o. for 10 days) using female rats.  Again, M. oleifera elicited significant increases in serum T4 with concomitant decreases in serum T3 and T3:T4 ratio but the hepatic indicator of lipid peroxidation and hepatic activities of SOD and catalase were unaffected by the higher dose.  The effects of M. oleifera on thyroidal hormones was postulated to involve inhibition of hepatic type-I 5′-iodothyronine monodeiodinase which catalyse the removal of one iodine atom from the 5′- position of thyroxine to produce T3. [12]

A source of β-carotene activity


Fresh or dehydrated M. oleifera leaves are importance plant sources of vitamin A that should be considered for supplementary feeding programs. Both the fresh or dehydrated leaves produced an increase in food intake and weight gain in vitamin A-deficient rats that were comparable or superior to those of vitamin A-depleted animals that were fed synthetic vitamin A.  The feeding of the vitamin A-depleted rats with the fresh or dehydrated leaves led to significant increases in serum and liver levels of vitamin A although the magnitude of rise in serum vitamin A levels was somewhat lower than those seen in synthetic vitamin A fed rats.  The dehydrated state of the leaves was a better source of vitamin A than the fresh leaves which could be attributed to partial cooking of the former during the processes of blanching and sulphiting and to the reduction in the matrix effect as the dehydrated leaves were finely powdered. [4]

Hypolipidaemic activity


M. oleifera tender and semi-ripe fruits (200 mg/kg/day, p.o.) showed hypolipidaemic and anti-atherosclerotic effects, and reduced the body weights of rabbits fed with standard laboratory diet or with a hypercholesterolaemic diet for 120 days. The reference hypolipidaemic drug used was lovastatin (6 mg/kg/day, p.o.).  M. oleifera fruit reduced the serum total cholesterol, phospholipid, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), total lipids and cholesterol to phospholipid (C/P) ratio, cholesterol balance and atherogenic index in rabbits fed a hypercholesterolaemic diet which contained 5% cholesterol, 5% coconut oil and 90% standard laboratory diet as compared to controls.  In normal rabbits, M. oleifera elicited a decrease in the HDL levels as compared to controls while in hyper-cholesterolaemic rabbits, a significant increase in HDL levels was elicited. The HDL ratio (HDL/HDL-total cholesterol) was increased in the M. oleifera-treated group.  This is a desirable criteria for a hypocholesterolaemic agent as a higher ratio indicated a lower atherosclerotic risk.  M. oleifera lowered the total protein levels that were significantly raised by hypercholesterolaemia, while in normal rabbits, no change in the total proteins was seen.  [8]

The elevated C/P ratio seen in hypercholestrolamic rabbits was markedly reduced by M. oleifera.  Since a high C/P ratio is commonly associated with atherosclerosis, this points to a possible role of M. oleifera in reducing the incidence of atherosclerosis.  In hypercholesterolaemic rabbits but not in normal rabbits, M. oleifera decreased the lipid profile of the liver, heart and aorta.  The atherogenic index which is an indication of the deposition of foam cells, plaque, fatty infiltration or lipids in the heart, coronaries, aorta, liver and kidneys, was significantly reduced by M. oleifera. A higher atherogenic index points to a higher risk of oxidative damage in the organs above.  M. oleifera increased the faecal excretion of cholesterol and phospholipids into faeces.  This may contribute to its hypolipidaemic effect. [8]

Anti-herpes simplex virus (HSV1) activity

The aqueous extract of M. oleifera leaves specifically inhibited plaque formation induced by HSV-1.  The therapeutic index (CC50/EC50) for M. oleifera aqueous extract against HSV-1 was 8.8 (EC50 of 100.0±5.3 µg/mL, CC50 of 875±35 µg/mL).  The reference antiviral compound used was acyclovir.  M. oleifera aqueous extract was more effective to APr HSV-1 strain than against HSV-1 TK and wild-type 7401H strains to examine the effects of M. oleifera aqueous extract in cutaneous HSV-1 infection model in mice, the animals were orally administered with the extract (250 mg/kg per dose, which correspond to the doses of other traditional herbs used in humans) every 8 hours for 5 days after infection.  M. oleifera aqueous extract significantly delayed the development and progression of skin lesions and/or prolonged the mean survival times.  To further examine the antiviral effects of M. oleifera, HSV-1 infected mice were given the extract (250 mg/kg per dose) for 14 consecutive days via oral gavage.  Again, the development and progression of skin lesions were delayed, the mean survival times prolonged and the mortality of the infected mice was reduced as compared to controls.  The body weights of M. oleifera-treated mice and the controls were similar on days 7 and 14 indicating that the extract exerted no toxicity in these mice.  M. oleifera aqueous extract did not exhibit anti-poliovirus or anti-measles virus activity in vitro.  The results of this study indicate that M. oleifera may be a possible source of a plant extract for anti-herpes simplex virus infections. [9]

Hypoglycaemic activity

The 95% ethanolic extract of M. oleifera (a single dose of 250 mg/kg emulsified in 10% ethanol-water vehicle, p.o.) elicited a significant blood glucose lowering effect to close to normal fasting levels after 1 week of administration in alloxan (100 mg/kg body weight, i.p.) diabetic albino rats. [23]


The LD50 value for the aqueous and alcoholic extract of M. oliefera root wood in adult albino mice was found to be 2000 mg/kg body weight for both extracts. [5] A compound isolated from M. oleifera, pterygospermin, has a subcutaneous LD50 value in mice and rats of 350-400 mg/kg body weight. [8]

The effects of a methanolic extract of M. oleifera root on liver and kidney functions and hematological parameters in mice were studied by the intraperitoneal administration of weekly (35, 46, 70 mg/kg) and daily (3.5, 4.6, 7.0 mg/kg) doses of the root extract. Low and moderate dose levels (3.5 and 4.6 mg/kg) of the daily regiment and low dose level (35 mg/kg) of the weekly regiment did not alter the hematological parameters or adversely affected liver and kidney functions.  At moderate dose level (46 mg/kg) of the weekly regiment, serum aminotransferase and plasma cholesterol levels were significantly changed.  In addition to these changes, the high dose (70 mg/kg) of the weekly regiment changed total bilirubin, non protein nitrogen, blood urea and plasma protein.  The high dose of the daily regiment (7.0 mg/kg) and moderate and high doses of the weekly regiment (> 46 mg/kg body wt.) significantly increased white blood cell count and decreased the clotting time.  Thus, moderate to high doses (> 46 mg/kg body wt.) of M. oleifera methanolic root extract given weekly and high doses (7 mg/kg) given daily affected liver and kidney functions and hematological parameters while weekly doses of 35 mg/kg and daily doses of 3.5 and 4.6 mg/kg were without adverse effects. [24]

However, the leaves are commonly taken as a vegetable wherever it is grown including in Nigeria without evidence of toxicity. [10]

Clinical Data

Clinical Trials

No documentation

Adverse Effects in Human:

No documentation

Use in Certain Conditions

Pregnancy / Breastfeeding

No documentation

Age Limitations

No documentation

Chronic Disease Conditions

No documentation


Interactions with drugs

No documentation

Interactions with Other Herbs / Herbal Constituents

No documentation



No documentation

Case Reports

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  1) Botanical Info


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  2. Anwar F, Latif S, Ashraf M, Gilani AH. Moringa oleifera: A food plant with multiple medicinal uses. Phytother Res., 2007; 21(1):17-25.
  3. Freiberger CE, Vanderjagt DJ, Pastuszyn A, Glew RS, Mounkaila G, Millson M, Glew RH. Nutrient content of the edible leaves of seven wild plants from Niger. Plant Foods for Human Nutrition, 1988; 53: 57–69.
  4. Nambiar VS,  Seshadri S. Bioavailability trials of β-carotene from fresh and dehydrated drumstick leaves (Moringa oleifera) in a rat model.  Plant Foods for Human Nutrition, 2001; 56: 83–95.
  5. Guevara AP, Vargas C, Sakurai H, Fujiwara Y, Hashimoto K, Maoka T, Kozuka M, Ito Y, Tokuda H, Nishino H. An antitumor promoter from Moringa oleifera Lam. Mutat Res., 1999; 440(2):181-8.
  6. Ching LS, Mohamed S. Alpha-tocopherol content in 62 edible tropical plants. Jurnal of Agricultural Food Chem., 2001; 49(6):3101-5.
  7. Karadi RV, Gadge NB, Alagawadi KR, Savadi RV. Effect of Moringa oleifera Lam. root-wood on ethylene glycol induced urolithiasis in rats. J Ethnopharmacol., 2006; 105(1-2):306-11.
  8. Mehta LK, Balaraman R, Amin A.H, Bafna P.A, Gulati O.D. Effect of fruits of Moringa oleifera on the lipid profile of normal and hypercholesterolaemic rabbits.  Journal of Ethnopharmacology, 2003; 86:191–195.
  9. Lipipun V, Kurokawa M, Suttisri R, Taweechotipatr P, Pramyothin P, Hattori M, Shiraki K. Efficacy of Thai medicinal plant extracts against herpes simplex virus type 1 infection in vitro and in vivo. Antiviral Research, 2003; 60:175–180.
  10. Ghasi S, Nwobodo E, Ofili JO. Hypocholestrolemic effects of cride extract of leaf of Moringa Oleifera Lam in high-fat diet fed wistar rats. J Ethnopharmacol., 2000; 69(1):21-5.
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  12. Tahiliani P, Kar A. Role of Moringa oleifera leaf extract in the regulation of thyroid hormone status in adult male and female rats. Pharmacological Research, 1999; 41(3).
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  15. Ray K, Hazra R, Guha D. Central inhibitory effect of Moringa oleifera root extract: possible role of neurotransmitters. Indian J Exp Biol., 41(11): 2003;1279-84.
  16. Rathi BS, Bodhankar SL, Baheti AM. Evaluation of aqueous leaves of Moringa oleifera Linn for wound healing in albino rats. Indian J. Exp. Biol., 44(11): 2006; 898-901.
  17. Rao AV, Devi PU, Kamath R. In vivo radioprotective effect of Moringa oleifera leaves. Indian J. Exp. Biol., 39(9): 2001; 858-63.
  18. Nwosa MO, Okafor JI. Preliminary studies of the antifungal activities of some medicinal plants against Basidiobolus and some other pathogenic fungi. Mycoses, 38(5-6): 1995; 191-5.
  19. Murakami A, Kitazono Y, Jiwajinda S, Koshimizu K, Ohigashi H. Niaziminin, a thiocarbamate from the leaves of Moringa oleifera, holds a strict structural requirement for inhibition of tumor-promoter-induced Epstein-Barr virus activation. Planta Med. May, 64(4): 1998; 319-23.
  20. Lampronti I, Khan MT, Bianchi N, Ather A, Borgatti M, Vizziello L, Fabbri E, Gambari R. Bangladeshi medicinal plant extracts inhibiting molecular interactions between nuclear factors and target DNA sequences mimicking NF-kappaB binding sites. Med Chem., 1(4): 2005; 327-33.
  21. Costa-Lotufo LV, Khan MTH, Ather A, Wilke DV, Jimenez PC, Pessoa C, de Moraes MEA, de Moraes MO. Studies of the anticancer potential of plants used in Bangladeshi folk medicine. Journal of Ethnopharmacology, 99: 2005; 21–30.
  22. Bharali R, Tabassum J, Azad MR. Chemomodulatory effect of Moringa oleifera Lam, on hepatic carcinogen metabolising enzymes, antioxidant parameters and skin papillomagenesis in mice. Asian Pacific J. Cancer Prev., 4(2): 2003; 131-9.
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