Syzygium jambolanum and Cephalandra indica homeopathic preparations inhibit albumin glycation and protect erythrocytes: an in vitro study.

BACKGROUND: Diabetes mellitus is a common endocrine disorder characterized by hyperglycemia eventually resulting in long-term complications. Increased glycation of proteins is implicated in the pathogenesis of complications. For treatment of diabetes, Syzygium jambolanum and Cephalandra indica are frequently prescribed in homeopathy. However their role in glycation is not well elucidated. The present study aimed to evaluate the role of these homeopathic preparations in glycation induced structural modifications and further to examine their cellular protection ability. METHODS: In human erythrocytes, in vitro mother tincture and dilutions of S. jambolanum (Sj ф, 30c, 200c), C. indica (Ci ф, 30c, 200c) and standard antiglycator (AG) were compared and their antiglycation potential assessed by the estimating different markers of glycation (frcutosamines, carbonyls, bound sugar), structural modifications (free amino and thiol group). Phytochemical characterization (total phenolic, flavonoids and glycosides contents) was performed. RESULTS: The homeopathic preparations have different mode of action on albumin glycation modifications. Sj ф preparation demonstrated effective inhibition of all glycation, structural modifications except amino group protection. When dilutions were compared, Sj preparations showed reduction of glycation, structural modifications. All preparations showed significant erythrocyte protection. Sj ф preparation exhibited noteworthy antiglycation and cell protection ability as compared to AG. CONCLUSION: These homeopathic preparations especially Sj ф prevented glycation induced albumin modifications and subsequent toxicity in human eryrthrocytre in vitro. Further investigation of their potential as antiglycators is justified.

Potentized Mercuric chloride and Nux vomica facilitate water permeability in erythrocytes of a fresh-water catfish Clarius batrachus under acute ethanol intoxication.

OBJECTIVES: The primary biomolecular target of a homeopathic potency is unknown. If it is a plasma membrane protein such as water-channel protein, the drug would alter water permeation in cells. Therefore, the objective is to see if potentized homeopathic drugs like Mercuric chloride 30c and Nux vomica 30c could alter permeation of water through the erythrocytes of a fresh water fish under acute ethanol intoxication. LOCATION: The work was carried out in the Zoology Laboratory of Visva Bharati University, Santiniketan, West Bengal, India. SUBJECT: Live freshwater catfish. DESIGN: Erythrocytes collected from fish with and without ethanol intoxication were incubated in distilled water at 30 degrees C for 30 minutes with Ethanol 30c (control), Merc cor 30c (test 1), and Nux vomica 30c (test 2). Merc cor 30c and Nux vom 30c were prepared by successive dilution of the respective mother tinctures with 90% ethanol (1:100) followed by sonication at 20 kHz for 30 seconds in 30 steps. Ethanol 30c was prepared in the same way from 90% ethanol diluted with 90% ethanol. In another experiment, fish were pretreated with Ethanol 30c and Nux vom 30c followed by ethanol injection at 2 g/kg of body weight. Then their erythrocytes were tested in vitro with the same potencies. After centrifugation of blood samples, fluid part was removed, erythrocyte pellets dried in a BioChemical Oxygen Demand (BOD; Atlas Surgical, New Delhi, India) incubator at 90 degrees C for 12 hours and intracellular water content measured. RESULTS: Red blood cells (RBCs) from ethanol-injected fish permeated more water than those from normal fish. Water permeation was enhanced with Merc cor 30c and Nux vom 30c. RBCs from fish pretreated with Nux vom 30c imbibed more water in in vitro treatments than those from fish pretreated with Ethanol 30c. CONCLUSION: Because water channel proteins or aquaporins are mainly responsible for water transport through the plasma membrane of RBCs, it is thought that potentized drugs interact with these proteins, thereby facilitating water influx in the cells.

The inhibition of cholinesterases by pancuronium.

Pancuronium causes a powerful and highly selective inhibition of human serum cholinesterase in vitro. The inhibition was studied in serum from 14 individuals of both sexes (5-60 years of age) with normal reactions to suxamethonium. Pancuronium, in a concentration of 2.3 x 10(-7) M, caused a 50% inhibition of the enzymatic hydrolysis of acetylcholine, when this substrate was present in a concentration of 10 x 10(-3) M. The same I50 value was also found for a commercial preparation of human serum cholinesterase. The inhibition was reversible and competitive in type. Pancuronium inhibition of the acetylcholinesterase in human red blood cells and from the electric eel was more than one thousand times weaker. Thus pancuronium is one of the most selective inhibitors of serum cholinesterase described so far. The in vivo activity of the serum cholinesterase in four patients receiving pancuronium 0.1 mg/kg decreased, during the first 3 min, by 60-80%, from the pre-induction value. After this a slow recovery occurred with 40% depression remaining at 45 min after the injection. The tachycardia produced by pancuronium may be related to this selective inhibition of serum cholinesterase. It is suggested that relaxants which selectively inhibit serum cholinesterase also selectively block the cardiac muscarinic receptors.