Bronchodilator, vasodilator and spasmolytic activities of Cymbopogon martinii.

Cymbopogon martinii (Cm.Cr) is traditionally used in south Asian communities for the management of multiple ailments including gastrointestinal, respiratory and vascular disorders and the present study was undertaken to validate these folkloric uses. The application of a methanol extract of the plant (Cm.Cr) to isolated rabbit jejunum preparation exhibited relaxation through decrease in magnitude and frequency of spontaneous contractions. The Cm.Cr also exerted relaxant effect on high K(+) (80 mM) induced contractions in isolated rabbit jejunum preparations. The Cm.Cr and its dichloromethane (Cm.Dcm) and aqueous (Cm.Aq) fractions also caused concentration-dependent relaxation in spontaneous and K(+) (80 mM) induced contractions which are comparables to effects produced by verapamil. Cm.Cr caused shifting of the Ca(2+)-curves toward right, suggesting the presence of a Ca(2+) channel blocking activity. Subsequently, Cm.Cr, Cm.Dcm and Cm.Aq caused relaxation of CCh (1 µM) and K(+) (80 mM) induced contractions in isolated rabbit tracheal preparations, suggesting that the observed relaxant effect can be mediated through antimuscarinic and/or Ca(2+) channel blocking activities. Cm.Cr tested against phenylephrine (PE; 1 µM) and K(+) (80 mM) induced contractions exhibited partial relaxation of isolated rabbit aortic preparations. The above-mentioned studies provided a scientific basis for the folkloric use of Cymbopogon martini in the management of multiple ailments in traditional systems of medicines.

Bronchodilator, vasodilator and spasmolytic activities of methanolic extract of Myrtus communis L.

The present study was undertaken to validate some of the folkloric claims about the effectiveness of the use of a Myrtus communis L. crude methanol extract (Mc.Cr) in gastrointestinal, respiratory and vascular diseases. Mc.Cr caused complete relaxation of spontaneous and K⁺ (80 mM)-induced contractions in isolated rabbit jejunum. It caused right ward parallel shift of calcium concentration response curves. Mc.Cr exhibited relaxant effect on CCh- and K⁺ (80 mM)-induced contractions in isolated rabbit tracheal preparations. Furthermore, Mc.Cr caused relaxation of phenylephrine (1 µM)- and K⁺ (80 mM)-induced contractions in isolated rabbit aorta preparations. These effects were similar to verapamil, a standard calcium channel blocker. These findings could be the basis for explaining the spasmolytic, bronchodilator and vasodilator activities of the extract, through a possible calcium channel blocking activity.

Studies on the antihypertensive, antispasmodic, bronchodilator and hepatoprotective activities of the Carum copticum seed extract.

This study describes the antihypertensive, antispasmodic, bronchodilator and hepatoprotective activities of the aqueous-methanolic extract of Carum copticum Benth. seeds (CSE) to rationalize some of its traditional uses. CSE (3-100 mg/kg) caused a dose-dependent fall in arterial blood pressure in anaesthetized rats. In isolated rabbit aorta and jejunum preparations, CSE (0.1-3.0 mg/ml) caused an inhibitory effect on the K+-induced contractions. The calcium channel blocking (CCB) effect was confirmed when CSE shifted the Ca2+ dose-response curves (DRCs) to right similar to verapamil. In isolated guinea-pig tracheal preparations, it caused inhibition of carbachol and K+-induced bronchoconstriction at 0.1-1.0 mg/ml as well as shifted the dose-response curves (DRCs) of carbachol and histamine to the right with suppression of maximum response suggestive of non-specific bronchodilator effect mediated possibly through CCB. Pretreatment of rats with CSE (500 mg/kg orally for 2 days at 12 h intervals) prevented paracetamol (640 mg/kg) and CCl4 (150 ml/kg)-induced rise in serum alkaline phosphatase (ALP) and aminotransferases (AST and ALT). The same dose of CSE was able to prevent the CCl4-induced prolongation in pentobarbital-induced sleeping time in mice confirming its hepatoprotectivity. These results indicate the presence of calcium antagonist(s) in Carum copticum seeds and thus provides sound mechanistic basis for some of their folkloric uses.

Studies on the protective effects of caffeic acid and quercetin on chemical-induced hepatotoxicity in rodents.

Caffeic acid and quercetin, the well-known phenolic compounds widely present in the plant kingdom, were investigated for their possible protective effects against paracetamol and CCl4-induced hepatic damage. Paracetamol at the oral dose of 1 g/kg produced 100% mortality in mice while pretreatment of separate groups of animals with caffeic acid (6 mg/kg) and quercetin (10 mg/kg) reduced the death rate to 20% and 30%, respectively. Oral administration of sub-lethal dose of paracetamol (640 mg/kg) produced liver damage in rats as manifested by the significant (P<0.01) rise in serum levels of aminotransferases (aspartate transaminase (AST) and alanine transaminase (ALT)) compared to respective control values. The serum enzyme values were significantly (P<0.01) lowered on pretreatment of rats with either caffeic acid (6 mg/kg) or quercetin (10 mg/kg). Similarly, the hepatotoxic dose of CCl4 (1.5 ml/kg; orally) also raised significantly (P<0.05) the serum AST and ALT levels as compared to control values. The same dose of the caffeic acid and quercetin was able to prevent CCl4-induced rise in serum enzymes. Caffeic acid and quercetin also prevented the CCl4-induced prolongation in pentobarbital sleeping time confirming their hepatoprotectivity. These results indicate that caffeic acid and quercetin exhibited hepatoprotective activity possibly through multiple mechanisms.

Studies on preventive and curative effects of berberine on chemical-induced hepatotoxicity in rodents.

Berberis aristata is an edible plant employed in the South Asian Traditional Medicine, particularly its fruits being used as a tonic remedy for liver and heart. In this investigation, berberine, a known compound from this plant, was studied for its possible antihepatotoxic action in rats. Pretreatment of animals with berberine (4 mg/kg; orally twice daily for 2 days) prevented the acetaminophen- or CCl4-induced rise in serum levels of alkaline phosphatase (ALP) and aminotransaminases (AST and ALT), suggestive of hepatoprotection. Post-treatment with three successive oral doses of berberine (4 mg/kg every 6 h) reduced the hepatic damage induced by acetaminophen, while CCl4-induced hepatotoxicity was not modified, suggesting a selective curative effect against acetaminophen. Pretreatment of animals with a single oral dose of berberine (4 mg/kg) induced prolongation of the pentobarbital (60 mg/kg, i.p.)-induced sleeping time as well as increased strychnine (0.3 mg/kg; i.p.)-induced toxicity, suggestive of inhibitory effect on microsomal drug metabolizing enzymes, cytochrome P450s (CYPs).

Studies on antihypertensive and antispasmodic activities of methanol extract of Acacia nilotica pods.

A methanol extract of Acacia nilotica pods (AN) caused a dose-dependent (3-30 mg/kg) fall in arterial blood pressure. Treatment of animals with atropine abolished the vasodilator response of acetylcholine (ACh), whereas the antihypertensive effect of the plant extract remained unaltered. Phentolamine (an alpha-adrenergic blocker) abolished the vasoconstrictor effect of norepinephrine (NE), whereas pretreatment of the animal with AN, did not modify the NE response. These results indicate that the antihypertensive effect of plant extract is independent of muscarinic receptor stimulation or adrenoceptor blockade. In the in vitro studies, AN produced a dose-dependent (0.3-3.0 mg/mL) inhibitory effect on force and rate of spontaneous contractions in guinea-pig paired atria. Similarly, it inhibited the spontaneous contraction of rabbit jejunum in a concentration-dependent (0.1-3.0 mg/mL) manner. AN also inhibited K(+)-induced contractions in rabbit jejunum at a similar concentration range, which suggests that the antispasmodic action of AN is mediated through calcium channel blockade, and this may also be responsible for the blood pressure lowering effect of AN, observed in the in vivo studies.

Possible mechanism of selective inotropic activity of the n-butanolic fraction from Berberis aristata fruit.

Berberis aristata is an edible plant employed in South Asian traditional medicine; in particular, its fruit is used as a tonic remedy for liver and heart. In isolated cardiac tissues, Berberis aristata fruit extract exhibits a positive inotropic action. Activity-directed fractionation using organic solvents revealed that the cardiotonic activity is concentrated in the n-butanolic fraction (BF). The cardiac action of BF was investigated in spontaneously beating right atria and in electrically driven right ventricular strips and left atria obtained from reserpinized guinea pigs. The results show that this fraction produces a dose-dependent positive inotropic action with little effect on heart rate. To study its possible mode of action, guinea pig atria were pretreated with propranolol, a beta-adrenoceptor blocking agent. This treatment abolished the cardiotonic effect of isoprenaline, whereas the cardiotonic effect of BF remained unaltered, suggesting that this effect does not involve stimulation of beta-adrenoceptors. On the other hand, application of carbachol reverses only part of the BF-induced increase in ventricular force of contraction, indicating that besides a cyclic AMP (cAMP)-dependent mechanism, a cAMP-independent mechanism underlies the inotropic action of BF. This is in line with the observation that the dynamics of isometric twitch contractions are not significantly altered by BF. Investigations in skinned myocardial preparations showed that BF modulates the calcium-dependent interaction of actin and myosin, apparently by reducing the cooperativity of the calcium-dependent binding of myosin to actin, i.e., there is enhanced calcium activation at low to physiological intracellular calcium, and reduced calcium activation at high intracellular calcium concentrations as present, for example, in ischemic calcium overload. These data indicate that the edible plant, Berberis aristata, contains active principle(s) that cause(s) a selective inotropic effect, involving-in the form of the modulatory effect on actin myosin cooperativity-a novel mechanism of action. Further phytochemical and pharmacological studies may lead to isolation and structural identification of an attractive, new cardiotonic agent from Berberis aristata fruit.

Potentiation of paracetamol and carbon tetrachloride-induced hepatotoxicity in rodents by the food additive vanillin.

The potential of vanillin to potentiate the paracetamol and carbon tetrachloride (CCl4)-induced hepatotoxicity was investigated in rats. Vanillin when given alone (15 mg/kg, orally), did not modify liver function in rats as the values of serum enzymes of alkaline phosphatase (ALP) and aminotransaminases (AST and ALT) were found similar to those in the normal animals. However, when given repeatedly before the administration of the subtoxic dose of paracetamol (500 mg/kg) or CCl4 (1 ml/kg), vanillin caused liver damage, as manifested by the significant increase in the serum levels of hepatic enzymes. When tested for its possible interaction with pentobarbital (75 mg/kg, i.p.) and strychnine (0.9 mg/kg, i.p.), it caused reduction in pentobarbital-induced sleep in mice as well as preventing the animals against the lethal effect of strychnine, suggestive of an induction of microsomal drug metabolizing enzymes. These results indicate that vanillin potentiates the hepatotoxic potential of paracetamol and CCl4 in rats probably through an enzyme induction process.

An assessment of the potential of protopine to inhibit microsomal drug metabolising enzymes and prevent chemical-induced hepatotoxicity in rodents.

The potential of protopine to inhibit microsomal drug metabolising enzymes (MDM E) and prevent paracetamol- and CCl4-induced hepatotoxicity was studied in rats. Paracetamol at the dose of 640 mg kg-1 produced hepatic damage in rats as manifested by the rise in serum levels of aspartate transaminase (AST) and alanine transaminase (ALT) to 972+/-186 and 624+/-131 IU (mean+/-sem; n=10), respectively, compared to respective control values of 101+/-29 and 64+/-18 IU. Pretreatment of rats with protopine (11 mg kg-1, orally twice daily for 2 days) lowered significantly the respective serum AST and ALT levels (P<0.05) to 289+/-52 and 178+/-43 IU. The hepatotoxic dose of CCl4 (1.5 ml kg-1; orally) raised serum AST and ALT levels to 543+/-89 and 387+/-69 IU (mean+/-sem; n=10), respectively, compared to respective control values of 98+/-28 and 56+/-17 IU. The same dose of protopine (11 mg kg-1) was able to prevent significantly (P<0.05), the CCl4-induced rise in serum enzymes and the estimated values of AST and ALT were 168+/-36 and 93+/-28 IU, respectively. Protopine caused prolongation (P<0.05) in pentobarbital (55 mg kg-1)-induced sleep as well as potentiated strychnine-induced toxicity in rats, suggestive of an inhibitory effect on MDME. These results indicate that protopine exhibits anti-hepatotoxic action which may be mediated through inhibition of MDME.

Esculetin prevents liver damage induced by paracetamol and CCL4.

Esculetin, a phenolic compound found in Cichorium intybus and Bougainvllra spectabillis was investigated for its possible protective effect against paracetamol and CCl4-induced hepatic damage. Paracetamol produced 100% mortality at the dose of 1 g kg-1 in mice while pre-treatment of animals with esculetin (6 mg kg-1) reduced the death rate to 40%. Oral administration of paracetamol (640 mg kg-1) produced liver damage in rats as manifested by the rise in serum enzyme levels of alkaline phosphatase (ALP) and aminotransferases (AST and ALT). Pre-treatment of rats with esculetin (6 mg kg-1) prevented the paracetamol-induced rise in serum enzymes. The hepatotoxic dose of CCl4 (1.5 ml kg-1; orally) also raised serum ALP, AST and ALT levels. The same dose of esculetin (6 mg kg-1) was able to prevent the CCl4-induced rise in serum enzymes. Esculetin also prevented CCl4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity. These results indicate that esculetin possesses anti-hepatotoxic activity and the presence of this compound in Cichorium intybus and Bougainvllra spectabillis may explain the folkloric use of these plants in liver damage.

Selective protective effect of an extract from Fumaria parviflora on paracetamol-induced hepatotoxicity.

1. The hepatoprotective activity of an aqueous-methanolic extract of Fumaria parviflora was investigated against paracetamol- and CCI4-induced hepatic damage. 2. Paracetamol (1 g/kg; orally) produced 100% mortality in mice; pretreatment of animals with the plant extract (500 mg/kg; orally) reduced the death rate to 50%. 3. Pretreatment of rats with plant extract (500 mg/kg, orally twice daily for 2 days) prevented (P < 0.001) the paracetamol (640 mg/kg)-induced rise in serum enzymes alkaline phosphatase (ALP) and transaminases (GOT and GPT), whereas the same dose of the extract was unable to prevent (P > 0.05) the CCI4-induced rise in serum enzyme levels. 4. Posttreatment with 3 successive doses of the extract (500 mg/kg, 6 hourly) also restricted the paracetamol-induced hepatic damage. 5. The plant extract (500 mg/kg; orally) caused significant prolongation in pentobarbital (75 mg/ kg)-induced sleep as well as increased strychnine-induced lethality in mice (P < 0.05), suggestive of an inhibitory effect on microsomal drug metabolizing enzymes (MDME). 6. It is conceivable therefore, that Fumaria parviflora extract exhibits a selective protective effect against paracetamol-induced hepatotoxicity, probably mediated through MDME inhibition.

The effect of caffeine on the pharmacokinetics of acetaminophen in man.

The influence of caffeine (60 mg) was studied on the pharmacokinetic characteristics of acetaminophen (500 mg single dose) in ten healthy male human volunteers in a complete cross-over design. A high-performance liquid chromatography (HPLC) method was used to analyse serum drug concentrations. Caffeine caused a highly significant (p < 0.01) increase in AUC and AUMC, a significant (p < 0.05) increase in Cmax, and a significant (p < 0.05) decrease in clearance (C1/F) of acetaminophen. We conclude that caffeine taken in doses commonly available commercially or in a cup of coffee can significantly potentiate the therapeutic potential of acetaminophen in man.

Evaluation of the protective potential of Artemisia maritima extract on acetaminophen- and CCl4-induced liver damage.

The hepatoprotective activity of the aqueous-methanolic extract of Artemisia maritima was investigated against acetaminophen (paracetamol, 4-hydroxy acetanilide)- and carbon tetrachloride (CCl4)-induced hepatic damage. Acetaminophen produced 100% mortality at the dose of 1 g/kg in mice, while pretreatment of animals with the plant extract (500 mg/kg) reduced the death rate to 20%. Acetaminophen at the dose of 640 mg/kg produced liver damage in rats as manifested by the significant (P < 0.001) rise in serum levels of glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) to 1529 +/- 172 I.U./l and 904 +/- 116 I.U./l (n = 10), respectively, compared to respective control values of 87 +/- 12 I.U./l and 31 +/- 5 I.U./l. Pretreatment of rats with the plant extract (500 mg/kg) lowered significantly (P < 0.001) the respective serum GOT and GPT levels to 112 +/- 10 I.U./l and 47 +/- 11 I.U./l. Similarly, a hepatotoxic dose of CCl4 (1.5 ml/kg, orally) raised significantly (P < 0.01) the serum GOT and GPT levels to 463 +/- 122 I.U./l and 366 +/- 58 I.U./l (n = 10), respectively, compared to respective control values of 92 +/- 18 I.U./l and 35 +/- 9 I.U./l. The same dose of plant extract (500 mg/kg) was able to prevent significantly (P < 0.01) the CCl4-induced rise in serum transaminases and the estimated values of GOT and GPT were 105 +/- 29 I.U./l and 53 +/- 17 I.U./l, respectively. Moreover, it prevented CCl4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity and validates the traditional use of this plant against liver damage.

Studies on protective effect of Cyperus scariosus extract on acetaminophen and CCl4-induced hepatotoxicity.

1. The hepatoprotective activity of aqueous-methanolic extract of Cyperus scariosus (Cyperaceae) was investigated against acetaminophen and CCl4-induced hepatic damage. 2. Acetaminophen produced 100% mortality at a dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 30%. 3. Acetaminophen at a dose of 640 mg/kg produced liver damage in rats as manifested by the rise in serum levels of alkaline phosphatase (ALP), glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) to 430 +/- 68, 867 +/- 305 and 732 +/- 212 IU/l (n = 10) respectively, compared to respective control values of 202 +/- 36, 59 +/- 14 and 38 +/- 7. 4. Pretreatment of rats with plant extract (500 mg/kg) significantly lowered (P < 0.05) the respective serum ALP; GOT and GPT levels to 192 +/- 31, 63 +/- 9 and 35 +/- 8. 5. The hepatotoxic dose of CCl4 (1.5 ml/kg; orally) raised serum ALP, GOT and GPT levels to 328 +/- 30, 493 +/- 102 and 357 +/- 109 IU/l (n = 10) respectively, compared to respective control values of 177 +/- 21, 106 +/- 15 and 47 +/- 12. 6. The same dose of plant extract (500 mg/kg) was able to significantly prevent (P < 0.05) CCl4-induced rise in serum enzymes and the estimated values of ALP, GOT and GPT were 220 +/- 30, 207 +/- 95 and 75 +/- 38, respectively. 7. The plant extract also prevented CCl4-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Preventive and curative effects of Artemisia absinthium on acetaminophen and CCl4-induced hepatotoxicity.

1. Effect of aqueous-methanolic extract of Artemisia absinthium (Compositae) was investigated against acetaminophen- and CCl4-induced hepatic damage. 2. Acetaminophen produced 100% mortality at the dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 20%. 3. Pretreatment of rats with plant extract (500 mg/kg, orally twice daily for two days) prevented (P < 0.01) the acetaminophen (640 mg/kg) as well as CCl4 (1.5 ml/kg)-induced rise in serum transaminases (GOT and GPT). 4. Post-treatment with three successive doses of extract (500 mg/kg, 6 hr) restricted the hepatic damage induced by acetaminophen (P < 0.01) but CCl4-induced hepatotoxicity was not altered (P > 0.05). 5. Plant extract (500 mg/kg) caused significant prolongation (P < 0.05) in pentobarbital (75 mg/kg)-induced sleep as well as increased strychnine-induced lethality in mice suggestive of inhibitory effect on microsomal drug metabolizing enzymes (MDME). 6. These results indicate that the crude extract of Artemisia absinthium exhibits hepatoprotective action partly through MDME inhibitory action and validates the traditional use of plant in hepatic damage.

Acetylation percentage method for determination of acetylator status in human volunteers and tuberculous patients.

Acetylation percentage method described here is rapid and economical. A comparison has been made between plasma half life (t (1/2)), acetylation ratio and acetylation percentage methods for the determination of phenotyping. Isoniazid (INH) was selected as a test drug. In 120 healthy volunteers and 60 tuberculosis patients, acetylation percentage method has been found simple and reliable as compared to the other methods.

Possible presence of calcium channel blocker(s) in Rubia cordifolia: an indigenous medicinal plant.

Crude extract of Rubia cordifolia (RC) was tested in isolated tissue preparations for its possible calcium channel antagonistic activity. RC suppressed the spontaneous contractions of guinea-pig atria, rabbit jejunum and rat uterus in a concentration dependent manner (0.1-3 mg/ml). In rabbit aorta, it inhibited norepinephrine (10 microM) and KCl (80 mM) induced contractions. Replacement of physiological salt solution with calcium free solution abolished the spontaneous movements of rabbit jejunum. However, addition of calcium (25 micrograms/ml) in the tissue bath restored the spontaneous movements. When the tissues were pretreated with plant extract (1 mg/ml) or verapamil (0.5 microgram/ml), addition of calcium failed to restore spontaneous contractions. These results indicate that the plant extract exhibits spasmolytic activity similar to that of verapamil suggestive of presence of calcium channel blocker like constituent(s) in this plant.

Hepatoprotective effects of artemisia scoparia against carbon tetrachloride: an environmental contaminant.

The hepatoprotective activity of crude extract of artemisia scoparia (aerial parts) was investigated against experimentally produced hepatic damage using carbon tetrachloride (CCl4) as a model hepatotoxin. CCl4 at the dose of 1.5 ml/kg, produced liver damage in rats as manifested by the rise in serum levels of AST and ALT to 395 +/- 110 and 258 +/- 61 IU/l (mean +/- SEM; n = 10) respectively, compared to control values of 106 +/- 15 and 26 +/- 04. Pretreatment of rats with plant extract (150 mg/kg) significantly lowered (P < 0.01), the respective serum GOT and GPT levels to 93 +/- 05 and 27 +/- 03 IU/l, indicating hepatoprotective action. Pentobarbital sodium (75 mg/kg)-induced sleeping time in mice was found to be 140.8 +/- 1.5 min (n = 10) which was similar (P > 0.05) to that obtained in the group of animals pretreated with the plant extract (139.9 +/- 1.8 min). CCl4 treatment extended the pentobarbital sleeping time to 212.2 +/- 19.1 min and pretreatment of animals with plant extract reversed the CCl4-induced prolongation in pentobarbital sleeping time to 143.9 +/- 5.5 min (P < 0.001) which further confirms the protective action of the plant extract against CCl4-induced liver damage. These data indicate that the plant artemisia scoparia is hepatoprotective and validate the folkloric use of this plant in liver damage.

Evaluation of the liver protective potential of Cichorium intybus seed extract on Acetaminophen and CCl(4)-induced damage.

The hepatoprotective activity of aqueous-methanolic extract of Cichorium intybus seeds was investigated against acetaminophen and CCl(4)-induced hepatic damage. Acetaminophen produced 100% mortality at the dose of 1 g/kg in mice while pretreatment of animals with plant extract (500mg/kg) reduced the death rate to 30%. Acetaminophen at the dose of 640 mg/kg produced liver damage in rats as manifested by the significant (P < 0.01) rise in serum levels of alkaline phosphatase (ALP), GOT and GPT to 393 ± 28, 767 ± 215 and 692 ± 191 IU/L (n = 10) respectively, compared to respective control values of 198 ± 15, 76 ± 07 and 39 ± 09. Pretreatment of rats with plant extract (500 mg/kg) significantly lowered (P < 0.01), the respective serum ALP, GOT and GPT levels to 228 ± 16, 68 ± 10 and 41 ± 08. Similarly, a hepatotoxic dose of CCl(4) (1.5 mL/kg; orally) significantly raised (P < 0.01), the serum ALP, GOT and GPT levels to 312 ± 20, 503 ± 98 and 407 ± 109 IU/L (n = 10) respectively, compared to respective control values of 215 ± 16, 79 ± 18 and 49 ± 10. The same dose of plant extract (500 mg/kg) was able to prevent significantly (P < 0.05) the CCl(4)-induced rise in serum enzymes and the estimated values of ALP, GOT and GPT were 222 ± 27, 114 ± 23 and 68 ± 14 respectively. Moreover, it prevented CCl(4)-induced prolongation in pentobarbital sleeping time confirming hepatoprotectivity and validates the folkloric uses of this plant in liver damage.