How Can Traditional Ethopian Medicine Help Against Diarrhea? Antidiarrheal and Antispasmodic Avtivities of Stephania Abyssinica (Minispermaseae)

Table of Contents

pages

Acknowledgement

List of Abbreviations

List of Tables

List of Figures

Abstract

1. Introduction
1.1 Overview of diarrhea
1.2 Normal Physiology
1.2.1 Absorption, Secretion and GI motility
1.2.2 Regulation of absorption, secretion and GI motility
1.3 Pathophysiology of diarrhea
1.3.1 General aspect
1.3.2 Pathophysiology of chronic diarrhea
1.4 Principles of diarrhea management
1.5 Antimotility, antisecretory and antispasmodic agents
1.6 Herbal remedies for GI motility disorders and use of S. abyssinica

2 Objectives of the study
2.1 General objective
2.2 Specific objectives

3. Materials and Methods
3.1 Drugs and chemicals
3.2 Plant material
3.3 Extraction of Plant material
3.4 Animal preparation and dosing
3.5Castor oil induced diarrheal model
3.6 In vivo GI motility test
3.7 Enteropooling test
3.8 In vitro antispasmodic test
3.9 Statistical analysis

4 Results
4.1 Effect of extract on castor oil induced diarrheal model in mice
4.2 Effect of the extract on GI motility
4.3 Effect of the extract on intestinal fluid accumulation
4.4 In-vitro antispasmodic activities of the extract

5 Discussion

6 Conclusion and Recommendation

Reference

Acknowledgement

My sincere gratitude goes to my advisor Dr. Ephrem Engidawork whose advice and support, from beginning to the end made me accomplish this work. I must thank Prof. Yalemtsehay Mekonnen for advice provided and allowing to use premises and facilities at biomedical laboratory of the biology department and I also appreciate the assistance of other staff of the biology department who extended technical support.

I would like to express my deepest gratitude to my family, and those friends who in one way or the other contributed to the accomplishment of this work.

Finally I thank School of Graduate Studies for funding this project

List of Abbreviations

Abbildung in dieser Leseprobe nicht enthalten

List of Tables

Table 1: Effects of methanol extract of S. abyssinica on castor oil induced diarrheal model in mice

Table 2: Effects of aqueous extracts of S. abyssinica on castor oil induced diarrheal model on mice

Table 3: Inhibitory effect the extract of S. abyssinica on normal GI transit of mice

Table 4: Inhibitory effect of the extract of S. abyssinica on castor oil induced intestine transit in mice

Table5: In-vivo antidiarrhea index of the extract in mice

Table 6: Effects of the extract of S. abyssinica on intestinal fluid accumulation of mice

List of Figures

Figure 1: In vivo Antidiarrheal index (ADI) of the extract

Figure 2: Effects of increasing concentration of SALM on the DRC of acetylcholine on guinea-pig ileum

Figure 3: Effects of increasing concentration of SALA on the DRC of acetylcholine on guinea-pig ileum

Abstract

Diarrhea is a leading cause of morbidity and mortality in developing countries. Diarrhea may result from disturbance in bowel function in which case there is increased bowel transit, excessive intestinal secretion of water and electrolytes, decreased intestinal reabsorptions as well as more frequent defecations of loose, watery stool.

Many plant preparations have claimed activities and traditional used as antidiarrhea and antispasmodic. S. abyssinica is traditionally used for treatment of diarrhea and stomachache in Ethiopia. The aim of this work was to evaluate the antidiarrheal and antispasmodic activities of the aqueous and methanol extract of the root and leaf of S. abyssinica.

Antidiarrheal activities were studied in mice using castor oil-induced diarrhea at doses of 25, 50,100, and 200 mg/kg body weight. The extracts significantly prolonged the time of diarrheal induction, increased diarrhea free time, reduced the frequency of diarrhea episodes, decreased the weight of stool, and decreased general diarrheal score in a dose dependent way. With dose of 200 mg/kg the extracts produced higher in-vivo antidiarrheal index (ADI) than the reference loperamide. ADI of loperamide, SALM, SALA, SARM and SARA was 77.33, 88.79, 89.21, 91.08 and 82.23, respectively.

In Entropooling test in mice the extract significantly (p < 0.01) inhibited intestinal fluid accumulations of mice in a dose dependent fashion; with dose of 100 mg/kg from1.03±0.093 ml of the control to 0.403±0.019ml, 0.210±0.018 ml, 0.494±0.012ml and 0.288±0.026ml by SALM, SARM, SALA and SARA respectively.

The antispasmodic activity studies were performed as in vitro and in vivo models. The in-vitro antispasmodic activity studies were performed on isolated GPI. The methanol and aqueous extracts of the leaf showed significant and concentration dependent inhibition of acetylcholine induced contraction of isolated GPI. The extracts depressed Emax of Ach, and decreased PD2 value of the Ach. The Emax of Ach at conc of 10-3M is decreased (from100 for the control group) by SALM with concentration of 200 and 100 ug/ml to 45.6±2.13 and 73.2±3.04 respectively, whereas by SALA with 200 and 100 ug/ml to 62.0±2.98 and 74.8±2.46 respectively.

In the in vivo antispasmodic activity test, the extract significantly decreased the peristaltic index (PI). In normal transit test, the PI of SALM, SALA, SARM and SARA with dose of 200 mg/kg was all 0.00 (100% suppression of normal peristalsis). However in castor oil induced transit with dose of 200 mg/kg the peristaltic index (PI) of SALM, SALA, SARM and SARA was 26.67, 36.85, 22.00 and 40.65 respectively.

The result of this study indicated that the plant extract possesses antidiarrheal and antispasmodic activities and proves the fact that this plant is used in traditional medicine for treatment of diarrhea, stomachache and abdominal cramp.

Key words: S. abyssinica, antidiarrheal, antispasmodic, antienteropooling, aqueous and methanol extract, animal (mice or guinea pig)

1. INTRODUCTION

1.1 Overview of diarrhea

Diarrhea is an increased frequency and decreased consistency of fecal discharge as compared with an individual's normal bowel pattern. Frequency and consistency are variable within and between individuals. For example, some individuals defecate as many as 3 times a day, while others defecate only 2 or 3 times per week (Barbara, 2006).

Diarrhea is loosely defined as passage of abnormally liquid or unformed stools at an increased frequency. For adults on a typical Western diet, stool weight >200 g/d can generally be considered diarrheal. Because of the fundamental importance of duration to diagnostic considerations, diarrhea may be further defined as acute if <2 weeks, persistent if 2 to 4 weeks, and chronic if >4 weeks in duration. Conditions, usually associated with the passage of stool totaling <200 gram/day, must be distinguished from diarrhea, as diagnostic and therapeutic algorithms differ (David and Camiller, 2004; Barbara, 2006).

Diarrhea is a leading cause of morbidity and mortality, especially among children in developing countries and it is a major health problem in children under 5 years (Gilani et al., 2005). The World Health Organization (WHO) has estimated that 3-5 billion cases occur each year (1 billion in children less than 5 years old) and about 5 million deaths are due to diarrhea (2.5 million in children, less than 5 years old) (Estrada-Soto et al., 2007).

From a mechanistic perspective, diarrhea can be caused by an increased osmotic load within the intestine resulting in retention of water within the lumen; excessive secretion of electrolytes and water into the intestinal lumen; exudation of protein and fluid from the mucosa and altered intestinal motility resulting in rapid transit and decreased fluid absorption. In most instances, multiple processes are affected simultaneously leading to a net increase in stool volume and weight accompanied by increase in fractional water content (Pasricha, 2006).

The major impact of these illnesses is morbidity, because it demands primary medical services, hospital-care time and labor days lost. Furthermore, the most highly used drugs for intestinal disease therapies are very expensive, overused and inadequate use of antibiotics has led to increased prevalence of multi drugs-resistant pathogens. Despite the etiology, chronic diarrhea is linked with dehydration and electrolyte-containing solutions are the first choice for treatment (Estrada-Soto et al, 2007).

Despite the availability of a vast spectrum of approaches for diarrheal management, majority of the population in the developing countries rely on herbal drugs for the management of diarrhea. Medicinal herbs constitute an indispensable component of the traditional medicine practiced worldwide due to the economical viability, accessibility, acceptability and ancestral experience (Afroz et al., 2006).

1.2 Normal physiology

The human small intestine and colon perform important functions including the secretion and absorption of water and electrolytes, the storage and subsequent transport of intraluminal contents. Alterations in fluid and electrolyte handling contribute significantly to diarrhea. Alterations in motor and sensory functions of the human colon result in highly prevalent syndromes such as irritable bowel syndrome, chronic diarrhea, and chronic constipation (David and Camiller, 2004).

The small intestine and colon have intrinsic and extrinsic innervation. The intrinsic innervation, also called the enteric nervous system (ENS), comprises myenteric, submucosal, and mucosal neuronal layers. The function of these layers is modulated by interneurons through the actions of neurotransmitter amines or peptides, including acetylcholine, opioids, norepinephrine, serotonin, ATP, and nitric oxide. The myenteric plexus regulates smooth muscle function, and the submucosal plexus affects secretion and absorption.The extrinsic innervations of the small intestine and colon are part of the autonomic nervous system and also modulate both motor and secretory functions. The chief excitatory neurotransmitters controlling motor function are acetylcholine and the tachykinins, such as substance P (Camiller and Murray, 2001; David and Camiller, 2004).

1.2.1 Absorption, secretion and GI motility

Sugars and amino acids are absorbed across the small-intestinal brush border membrane via carriers that couple their movements to that of Na+. Na+ coupling permits the organic solute to be transported uphill, i.e., from low luminal to higher cell concentration, a gradient opposite to that for Na+. The organic solutes then move downhill from enterocyte to blood via basolateral membrane carriers that operate independently of ion movements (Schultz et al., 1966; Ganapath et al., 1985).

The Na+ gradient, therefore, is the driving force for amino acid, oligopeptide, and sugar absorption. As these organic solutes are absorbed, salt is absorbed with them, and water follows osmotically transport from enterocyte to lateral intercellular space creates a local osmotic gradient that initiates water flow. The coupled transport of Na+ and organic solute is the theoretical basis for oral rehydration therapy in severe diarrhea (Schultz et al., 1966; Ganapath et al., 1985).

Normally about 8 to 9 liters of fluid enter the small intestine daily from exogenous and endogenous (secretion) sources. Net absorption of the water occurs in the small intestine in response to osmotic gradients that result from the uptake and secretion of ions and the absorption of nutrients (mainly sugars and amino acids), with only about 1 to 1.5 liters crossing the ileocecal valve. The colon then extracts most of the remaining fluid, leaving about 100 ml of fecal water daily (Pasricha, 2006).

Secretions in intestine has role in duodenal alkalinization. The ion exchangers that are localized in small-intestinal and colonic brush border membranes play this role. The individual cell membrane transporters contributing to active Cl- secretion the three membrane proteins involved are: the apical anion channel, the basolateral membrane K+ channel and the basolateral membrane NaK2Cl cotransporter (Micheal et al., 2003).

GIT also do two types of motility under autonomic control as fed state (peristalsis) and fast state. This motility ensures the mixing of ingested food and let the bolus in one part of the GI move to the other part. It also works housekeeping activities by moving out the unabsorbed debris out of the GIT (Pasricha, 2006).

1.2.2 Regulation of absorption, secretion and GI motility

The gastrointestinal tract is in a continuous contractile, absorptive, and secretory state. The control of this state is complex, with contributions by the muscle itself, local nerves (i.e., the enteric nervous system, ENS), the central nervous system (CNS), and humoral pathways. Of these, perhaps the most important regulator of physiological gut function is the ENS. Alterations in gastrointestinal motility and in the balance of absorption and secretion in the intestines may underlie irregularities in bowel habits. (Longstereth, 1998; Pasricha and Jefri, 2001).

The ENS is composed of interconnected networks of ganglion cells and nerve fibers mainly located in the submucosa (submucosal plexus) and between the circular and longitudinal muscle layers (myenteric plexus). These networks give rise to nerve fibers that connect with the mucosa and deep muscle. Although extrinsic sympathetic and parasympathetic nerves project onto the submucosal and myenteric plexuses, the ENS can independently regulate gastrointestinal motility and secretion (Mc Quid, 2007).

The neurons within the plexuses secrete different neurotransmitters and a variety of pharmacologically active peptides. The classes of compounds that stimulate active secretion and inhibit active absorption, and those with the opposite effects. The former group includes three kinds of agents: (a) neurotransmitters, including vasoactive intestinal peptide (VIP), acetylcholine, substance P, and the nucleotides ATP; (b) the paracrine agents serotonin and neurotensin, which are released by endocrine (enterochromaffin) cells in the intestinal epithelium; (c) agents released by inflammatory cells, including mainly prostaglandins, histamine, and serotonin (Sellin, 1993; Quigly et al., 1999; Range et al., 2003).

The group of compounds that both inhibit active secretion (HCO3- as well as Cl-) and enhance active absorption includes norepinephrine (via a2-receptors), neuropeptide Y, enkephalins, somatostatin, and paracrine agents (Sellin, 1993).

The basic motor tool used by the ENS to integrate its GI motility programs is the peristaltic reflex. Physiologically, peristalsis is a series of reflex responses to a bolus in the lumen of a given segment of the intestine; the ascending excitatory reflex results in contraction of the circular muscle on the oral side of the bolus, while the descending inhibitory reflex results in relaxation on the anal side. The net pressure gradient moves the bolus caudal (Furness and Sanger, 2002; Galligan, 2002).

Three neural elements, responsible for sensory, relay, and effector functions, are required to produce these reflexes. Luminal factors stimulate sensory elements in the mucosa, leading to a coordinated pattern of muscle activity that is directly controlled by the motor neurons of the myenteric plexus to provide the effector component of the peristaltic reflex (Furness and Sanger, 2002; Galligan, 2002; Pasricha, 2006).

Motor neurons receive input from ascending and descending interneurons (which constitute the relay and programming systems) that are of two broad types, excitatory and inhibitory. The primary neurotransmitter of the excitatory motor neurons is acetylcholine (ACh). The principal neurotransmitter in the inhibitory motor neurons appears to be nitric oxide (NO), although important contributions may also be made by ATP, and vasoactive intestinal peptide (VIP), all of which are variably co-expressed with NO synthase (Furness and Sanger, 2002; Galligan, 2002; Pasricha, 2006).

1.3 Pathophysiology of diarrhea

1.3.1 General aspects

Osmosis, active secretion, exudation, and altered motility can all drive diarrhea. Specific diarrheal illnesses often involve more than one of these forces.

i) Osmotic diarrhea: When poorly absorbable, low-molecular weight aqueous solutes are ingested, their osmotic force quickly pulls water and, secondarily, ions into the intestinal lumen. Individuals with normal gut function will develop osmotic diarrhea when they ingest large amounts of poorly absorbable solutes, such as lactulose (if they are being treated for hepatic encephalopathy), sorbitol (if they continually chew sugar-free gum), or Mg2+ (if they take certain antacids or bowel purgatives) (Micheal et al., 2003)
ii) Secretory diarrhea: Diarrhea resulting from overstimulation of the intestinal tract’s secretory capacity can develop in “pure” form (e.g., cholera) or as a component of a more complex disease process (e.g., celiac disease, Crohn disease). “Pure” secretory diarrhea is characterized by (a) large stool volumes (which can exceed 1 liter per hour in well hydrated adults), (b) absence of red or white blood cells in the stool, (c) absence of fever or other systemic symptoms (except those due to dehydration), (d) persistence of diarrhea with fasting (volume may diminish, however), and (e) lack of excess osmotic gap (OG) in stool electrolytes. Osmotic gap is defined as follows: OG = 290 - 2{[Na+] + [K+]}, where 290 is the assumed osmolarity of blood plasma. A gap greater than 50 mM is considered abnormal; the normal gap is made up of Mg2+, Ca2+, NH4+, and perhaps organic cations (Farthing et al., 2002; Micheal et al., 2003).

The pattern of stool electrolytes in patients with acute cholera shows Na+, K+, and Cl- concentrations not very different from those in plasma and HCO3- concentration somewhat higher than in plasma. In contrast, normal stool shows low [Na+] and high [K+] concentrations, due mainly to the colon’s reabsorption of Na+ and secretion (both active and passive) of K+; and a low [Cl-] concentration, due to the replacement of [Cl-] by short-chain organic acid anions generated by colonic bacteria. Normally, [HCO3-] concentration is similar to that in plasma (Farthing et al., 2002; Micheal et al., 2003).

iii) Exudative diarrhea: If the intestinal epithelium’s barrier function is compromised by loss of epithelial cells or disruption of tight junctions, hydrostatic pressure in blood vessels and lymphatics will cause water and electrolytes, mucus, protein, and sometimes even red and white cells to accumulate luminally (e.g., ulcerative colitis, shigellosis, intestinal lymphangiectasia). If the condition is chronic, the continuing protein loss can lead to hypoalbuminemia and hypoglobulinemia (Micheal et al., 2003; David and Camiller, 2004).
iv) Diarrhea resulting from motility disturbances: Both increases and decreases in gut motility can lead to diarrhea. Examples of the former are thyrotoxicosis and opiate withdrawal. Decreases in effective motility in the small intestine due to large diverticula, smooth muscle damage, or autonomic neuropathy (diabetic, idiopathic) can result in bacterial overgrowth. And bacterial overgrowth can lead to diarrhea (Chang et al., 1982).

1.3.2 Pathophysiology of chronic diarrhea

i) Hormone-secreting neoplasms: In several uncommon tumors, hormones are produced and released that directly stimulate intestinal secretion, causing profuse diarrhea or, in one instance (gastrinoma), interfering with nutrient absorption (Jensen et al., 1999).

In patients with pancreatic cholera, certain endocrine neoplasms that occur most commonly in pancreatic islets but occasionally in the proximal intestinal mucosa secrete large quantities of VIP, the enteric secretory neurotransmitter. Pheochromocytomas do so also. Profuse diarrhea develops in 30% of patients with medullary carcinoma of the thyroid because of secretion of calcitonin, another secretory stimulus in the intestine (Jensen et al., 1999; Camiller and Murray, 2001).

In Zollinger-Ellison syndrome (gastrinoma), both diarrhea and peptic ulceration can result from the marked increase in gastric acid production that is associated with gastrin- secreting neoplasms. About half of the patients with the rare neoplasm systemic mastocytosis develop diarrhea, likely due to histamine-induced gastric hypersecretion, a cause similar to that of the diarrhea in Zollinger-Ellison syndrome (Jensen et al., 1999; David and Camiller, 2004).

ii) Diabetes mellitus: Diarrhea accompanied by rectal incontinence is an occasional complication of long-standing, insulin-dependent diabetes. It typically occurs in patients with poor diabetic control and peripheral neuropathy. Intestinal biopsies in such patients are usually normal, and nutrient malabsorption or bacterial overgrowth is present only in a minority of cases. In most instances, the diarrhea is secondary to degeneration of adrenergic nerves in effect less noradrenalin, that, as mentioned above, are antisecretory and/or proabsorptive in intestinal fluid homeostasis (Chang et al., 1985).

1.4 Principles of diarrhea management

Many patients with sudden onset of diarrhea have a benign, self-limited illness requiring no treatment or evaluation. In severe diarrheal cases, dehydration and electrolyte imbalances are the principal risk, particularly in infants, children, and frail elderly patients. Oral rehydration therapy therefore is a cornerstone for patients with acute illnesses resulting in significant diarrhea. This therapy exploits the fact that nutrient- linked co-transport of water and electrolytes remains intact in the small bowel in most cases of acute diarrhea. Sodium and chloride absorption is linked to glucose uptake by the enterocyte; this is followed by movement of water in the same direction. A balanced mixture of glucose and electrolytes in volumes matched to losses therefore can prevent dehydration (Rang et al., 2003; Pasricha, 2006).

Pharmacotherapy of diarrhea should be reserved for patients with significant or persistent symptoms. Nonspecific antidiarrheal agents typically do not address the underlying pathophysiology responsible for the diarrhea; their principal utility is to provide symptomatic relief in mild cases of acute diarrhea. Many of these agents act by decreasing intestinal motility and should be avoided as much as possible in acute diarrheal illnesses caused by invasive organisms. In such cases, these agents may mask the clinical picture, delay clearance of organisms, and increase the risk of systemic invasion by the infectious organisms; they also may induce local complications such as toxic megacolon (Pasricha, 2006; Mc Quid, 2007).

For many chronic conditions, diarrhea can be controlled by suppression of the underlying mechanism. Examples include elimination of dietary lactose for lactase deficiency, use of glucocorticoids or other anti-inflammatory agents for idiopathic inflammatory bowel diseases, adsorptive agents such as cholestyramine for ileal bile acid malabsorption (David and Camiller, 2004).

Proton pump inhibitors such as omeprazole for the gastric hypersecretion of gastrinomas, somatostatin analogues such as octreotide for malignant carcinoid, prostaglandin inhibitors such as indomethacin for medullary carcinoma of the thyroid, and pancreatic enzyme replacement for pancreatic insufficiency. Clonidine, an a 2 adrenergic agonist, may allow control of diabetic diarrhea. For all patients with chronic diarrhea, fluid and electrolyte repletion is an important component (Camiller and Murray, 2001; David and Camiller, 2004).

1.5 Antimotility, antisecretory and antispasmodic agents

i) Opioid agonists: Opioid receptors (р,к, and 5) exist in high density in the GIT, located particularly in the myenteric and submucosal plexus, as well as on nociceptive pathways to the brain. In the stomach, motility (rhythmic contraction and relaxation) may decrease. In the small intestine resting tone (persistent contraction) is increased, with periodic spasms, but the amplitude of non propulsive contractions is markedly decreased. In the large intestine, propulsive peristaltic waves are diminished and tone is increased; this delays passage of the fecal mass and allows increased absorption of water, which leads to constipation (Szarka et al., 2007).

They act by several different mechanisms, mediated principally through either mu- or sigma-opioid receptors on enteric nerves, epithelial cells, and muscle. These mechanisms include effects on intestinal motility (p receptors), intestinal secretion (S receptors), or absorption (p and ô receptors) (Szarka et al., 2007).

ii) Chloride channel blockers are effective antisecretory agents in vitro but are too toxic for human use and have not proven to be effective antidiarrheal agents in vivo.

iii) Calcium channel blockers such as verapamil and nifedipine reduce motility and may promote intestinal electrolyte and water absorption. Constipation, in fact, is a significant side effect of these drugs. However, because of their systemic effects and the availability of other agents, they seldom if ever are used for diarrheal illnesses (Pasricha and Jefri, 2001; Pasricha, 2006).
iv) Berberine is a plant alkaloid used most commonly in bacterial diarrhea and cholera, but is also apparently effective against intestinal parasites. The antidiarrheal effects in part may be related to its antimicrobial activity, as well as its ability to inhibit smooth muscle contraction and delay intestinal transit by antagonizing the effects of acetylcholine (by competitive and noncompetitive mechanisms) and blocking the entry of Ca2+ into cells. In addition, it inhibits intestinal secretion (Pasricha, 2006).
v) Somatostatin analogues: Octreotide is an octapeptide analog of somatostatin that is effective in inhibiting the severe secretory diarrhea brought about by hormone-secreting tumors of the pancreas and the gastrointestinal tract. In hormone-secreting neoplasms, they block hormones (serotonin, VIP and gastrin) production by the tumor. Since they also appear to have a direct antisecretory effect on the gut epithelium, they have been employed for treating other forms of secretory diarrhea; cancer chemotherapy-induced diarrhea, diarrhea associated with human immunodeficiency virus (HIV), and diabetes- associated diarrhea (Jensen et al., 1999).
vi) Antispasmodics: The antispasmodics are considered useful for relieving or calming colicky pains resulting from spasms of the gut muscles and diarrhea due to hypermotility of the gastrointestinal tract (Gilani et al., 1994).

Abdominal pain is a major symptom in IBS, and clinicians have observed that anticholinergic drugs may provide temporary relief for symptoms such as painful cramps related to intestinal spasm. Although controlled clinical trials have produced mixed results, evidence generally supports beneficial effects of anticholinergic drugs (clidinium, prophantiline, dicyclomine and hyoscyamine) for pain (Tally et al., 2003). The most common agents of this class are nonspecific antagonists of the muscarinic receptor and include the tertiary amines dicyclomine and hyoscyamine, and the quaternary ammonium compounds glycopyrrolate and methscopolamine (Rang et al., 2003).

Antispasmodic agents relax smooth muscle in the gut and reduce contractions. They act through anticholinergic or antimuscarinic properties. The anticholinergic effects of antispasmodics limit their use, especially in the long term (Tally et al., 2003).

1.6 Herbal remedies for gastrointestinal motility disorders and use of Stephania abyssinica

Plants have been utilized as a medicine for thousands of years. More recently, a WHO study has shown that about 80% of the world’s population still relies on traditional medicine (Dharmani and Palit et al., 2006). A growing numbers of plants have been reported for antidiarrheal and antispasmodic activity.

Various herbal preparations have been used and claimed to have benefits as antidiarrheal and antispasmodic. Among these are Taverniera abyssinica , Syzygium guineese, Lipdium sitivium, Solaniase gigsa, Moringa stenopetala, Atropa belladonna, Berberis vulgaris, Evodia rutaecarpa, and Linum sitatissimum. And Studies were done to proof the traditional use the preparations (Abebe and Ayehu, 1993; Abebe et al., 2003).

Aqueous extract of the roots of Taverniera abyssinica (“Dengetegna”) antagonized Ach and histamine induced contractile responses of the guinea pig ileum and relaxed the smooth muscle of rabbit duodenum, which is suggesstive of its ethnomedical use in stomachache treatment (Noamesi et al., 1990). The antihistaminic and anticholinergic activities of aqueous extract of barberry fruits (Berberis vulgaris) were investigated on isolated guinea-pig ileum and the extract were found to possess anticholinergic and antihistaminic activities (Shamsa et al., 1999).

The leaf ethanol extract of Moringa stenopetala was shown to have a potential antispasmodic effect on guinea pig ileum (Mekonnen et al., 1999). The aqueous extract of Linum sitatissimum (“Telba”) seed was observed to show significant spasmolytic acivitiy and protective effects against experimental ulcerogenesis in guinea pig ileum and mouse stomach (Makonnen et al., 1996).

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