Bioactivity of methyl palmitate obtained from a mangroove plant Salvadora persica L

Abstract

The invention discloses a process of extracting, fractionating and purifying bioactive molecules from an associated mangrove plant, methods of screening for pharmacological activities of crude extract, its fractions and purified compounds and use of methyl palmitate obtained from the crude extract as a muscurine antagonist.

1 . A novel muscarine antagonist, comprising an effective amount of the compound methyl palmitate obtained from the mangrove plant  Salvadora persica.    
     
     
         2 . A composition as claimed in  claim 1 , wherein the composition inhibits gastric acidity on M1 receptor in the muscles of the stomach of rat.  
     
     
         3 . A composition as claimed in  claim 1 , wherein the composition shows activity on M3 receptors of guinea pig ileal and bladder detrusor muscles.  
     
     
         4 . A method for the treatment of muscurine disorders, comprising the step of administering an effective amount of methyl palmitate obtained from the plant  Salvadora persica.    
     
     
         5 . A method as claimed in  claim 4  wherein the muscurine disorders are such as renal colitis, motion sickness, abdominal cramps and bronchial asthma.  
     
     
         6 . A method as claimed in  claim 4  wherein the amount of methyl palmitate administered is 0.1 to 10 mg per kilogram of body weight.  
     
     
         7 . A process for producing methyl palmitate from a mangrove plant  Salvadora persica , said process comprising 
 (a) obtaining an extract from  Salvadora persica , and    (b) extracting and purifying the biologically active methyl palmitate from the extract.    
     
     
         8 . A process as claimed in  claim 7 , wherein the extract is prepared by: 
 (i) air-drying the plant parts;    (ii) immersing the plant parts in 90 percent aqueous methanol for one week at room temperature (28±2° C.);    (iii) filtering the methanolic extract by conventional methods; and    (iv) evaporating the methanolic extract at room temperature (28±2° C.) to obtain a crude extract.    
     
     
         9 . A process as claimed in  claim 8 , wherein the plant parts of  Salvadora persica  are selected from leaves, stems and flowers.  
     
     
         10 . A process as claimed in  claim 8 , wherein the extract is selected from chloroform extract, aqueous extract and hexane extract.  
     
     
         11 . A process as claimed in  claim 8 , wherein the extraction and purification of methyl palmitate is done by: 
 a) Obtaining the extract of  Salvadora persica;      b) testing the extract using methods of pharmacology;    c) fractionating the extract;    d) testing the fractions using methods of pharmacology;    e) isolating the pure methyl palmitate by any one of the conventionally known methods;    f) testing the pure compound by using methods of pharmacology; and    g) identifying the compound by any known method.    
     
     
         12 . A process as claimed in  claim 8  wherein methyl palmitate is capable of distinguishing between muscarinic receptors of atrium and other parts of the body and shows heterogeneity of muscarinic receptors.  
     
     
         13 . A process as claimed in  claim 8  wherein methyl palmitate inhibits gastric acidity and gastrointestinal disorders.  
     
     
         14 . A process as claimed in  claim 8  wherein methyl palmitate inhibits gastric acidity on M1 receptor of stomach of rat.  
     
     
         15 . A process as claimed in  claim 8  wherein methyl palmitate does not block M2 receptors and thereby does not have inhibitory effect on the contractions of atrial muscles of guinea pig in the dosage range used.  
     
     
         16 . A process as claimed in  claim 8  wherein methyl palmitate shows activity on M3 receptors of guinea pig ileal and bladder detrusor muscles.  
     
     
         17 . A process as claimed in  claim 8  wherein methyl palmitate produces a right shift of the dosage response curves of acetyl chlorine with the maximum response remaining the same.  
     
     
         18 . A process as claimed in  claim 8  wherein methyl palmitate shows competitive antagonism which is reversible in nature.  
     
     
         19 . A process as claimed in  claim 8  wherein methyl palmitate shows muscarinic activity with a milder potency than atropine.  
     
     
         20 . A method of treating gastric acidity and gastrointestinal disorders in mammals by administering methyl palmitate or an extract from a new mangrove plant source namely  Salvadora persica.    
     
     
         21 . A method as claimed in  claim 20  wherein the M1 receptor receive 0.1 to 10 mg of methyl palmitate per kilogram of body weight.  
     
     
         22 . A method as claimed in  claim 20  wherein methyl palmitate is administered for every 15 minutes.  
     
     
         23 . A method as claimed in  claim 20  wherein the M2 receptors receive 10×10 −6  to 400×10 −6  moles/ml of methyl palmitate.  
     
     
         24 . A method as claimed in  claim 20  wherein methyl palmitate is administered for every 10 minutes.  
     
     
         25 . A method as claimed in  claim 20  wherein the M3 receptors receive 50×10 −6  to 400×10 −6  moles/ml of methyl palmitate.  
     
     
         26 . A method as claimed in  claim 20  wherein methyl palmitate is administered for every 60 seconds.  
     
     
         27 . A method as claimed in  claim 20  wherein the M3 receptors are ileum and bladder.  
     
     
         28 . A method as claimed in  claim 20  wherein the inhibition of gastric acidity is directly proportional to the increase in the dosage.  
     
     
         29 . Use of methyl palmitate or an extract obtained from new mangrove plant source namely  Salvadora persica  as muscarine antagonist in mammals.  
     
     
         30 . Use as claimed in  claim 29  wherein methyl palmitate is capable of distinguishing between muscarinic receptors of atrium and other parts of the body and shows heterogeneity of muscarinic receptors.  
     
     
         31 . Use as claimed in  claim 29  wherein methyl palmitate is capable of inhibiting gastric acidity and gastrointestinal disorders.  
     
     
         32 . Use as claimed in  claim 29 , wherein methyl palmitate is capable of inhibiting gastric acidity on M1 receptor of stomach of rat.  
     
     
         33 . Use as claimed in  claim 29  wherein methyl palmitate does not block M2 receptors and thereby does not have inhibitory effect on the contractions of atrial muscles of guinea pig in the dosage range used.  
     
     
         34 . Use as claimed in  claim 29  wherein methyl palmitate shows activity on M3 receptors of guinea pig ileal and bladder detrusor muscles.  
     
     
         35 . Use as claimed in  claim 29  wherein methyl palmitate produces a right shift of the dosage response curves of acetyl chlorine with the maximum response remaining the same.  
     
     
         36 . Use as claimed in  claim 29  wherein methyl palmitate shows competitive antagonism, which is reversible in nature.  
     
     
         37 . Use as claimed in  claim 29  wherein methyl palmitate shows muscarinic activity with a milder potency than atropine.  
     
     
         38 . Use as claimed in  claim 29  wherein the M1 receptor receives 0.1 to 10 mg of methyl palmitate per kilogram of body weight.  
     
     
         39 . Use as claimed in  claim 29  wherein methyl palmitate is administered for every 15 minutes.  
     
     
         40 . Use as claimed in  claim 29  wherein the M2 receptors receive 10×10 −6  to 400×10 −6  moles/ml of methyl palmitate.  
     
     
         41 . Use as claimed in  claim 29  wherein methyl palmitate is administered for every 10 minutes.  
     
     
         42 . Use as claimed in  claim 29  wherein the M3 receptors receive 50×10 −6  to 400×10 −6  moles/ml of methyl palmitate.  
     
     
         43 . Use as claimed in  claim 29  wherein methyl palmitate is administered for every 60 seconds.