Vol.04, Issue 01, January 2019 Available Online: www.ajeee.co.in/index.php/AJEEE
A STUDY AND REVIEW ON PRECLINICAL SCREENING OF ERIOBOTRYA JAPONICA FRUITS EXTRACT FOR ANTIULCER AND TWIGS EXTRACT FOR DIURETIC ACTIVITY
IN EXPERIMENTAL RATS JV’n Nitin Kumar, Research Scholar
Dr. S.C. Mehta,
Guide, Jayoti Vidyapeeth Womens University, Jaipur, (Raj.) 1. INTRODUCTION
1.1 Gastric Ulcer
The stomach is a hollow, muscular, dilated part of the digestive system which functions as an essential organ of the digestive tract in many animals. In most vertebrates, the stomach is situated between the esophagus and the small intestine. It secretes protein-digesting enzymes called proteases and acid to help in food digestion, through smooth muscle contractions before transport of partially digested food (chyme) to the small intestines. Peptic ulcers are a profound gastrointestinal erosion disorder that involves the entire mucosal thickness, penetrating the muscular mucosa (Dharmani & Kuchibhotla, 2004). For decades it was believed that excessive secretion of gastric acid causes gastrointestinal ulceration, but many patients presenting such ulceration had standard acid secretion rates. Then, a researcher reported that peptic ulcers are triggered due to an imbalance between the aggressive factors and some known defense mechanism (Tarnowski AS., 2005). A wide variety of drugs are available for the treatment of peptic ulcer, but clinical evaluation of these drugs indicates high incidences of relapse, side effects, and drug interactions (Ahmad et al., 2013)
1.2 Symptoms
Many stomach ulcers are asymptomatic.
The signs of a stomach ulcer can include abdominal pain just below the ribcage.
The pain is usually worse after a meal or in the middle of the night when the stomach is empty.
• Nausea, vomiting
• Loss of weight, appetite
• Tiredness, weakness (a symptom of a bleeding ulcer)
• Blood present in vomit or stool.
When blood is in the stool, it appears tarry or black (a symptom of a bleeding ulcer) (Rubin &
Gorstein, 2005).
1.3 Risk Factors for Developing Peptic Ulcer Disease
A. Lifestyle Factors
• Some studies suggest that smoking can increase the risk of H. pylori and can slow the healing
of peptic ulcer
(www.ncbi.nlm.nih.gov/pubmed/1 0958211).
• Consumption of acidic drinks such as fruit juices and consuming caffeinated foods. Beverages can cause gastric irritation and increase production of gastric acid. It can make people more susceptible to H. pylori infection.
• Alcohol in large quantities can cause gastric irritation leading to increased susceptibility to H.
pylori.
• Alcohol consumption while using non-steroidal anti-inflammatory agents can further increase the chances of developing peptic ulcer.
• Even in the absence of alcohol misuse, some anti-inflammatory medicines (including aspirin and most other drugs commonly available over-the-counter or by prescription as “non steroidal”) can increase the risk of peptic ulcer. These drugs are responsible for at least half of all peptic Ulcer in elderly persons.
B. Helicobacter Pylori Infection
Infection with Helicobacter pylori is the most well-defined risk factor for the development of peptic ulcer (Wallace &
Granger, 1996) Age
Duodenal ulcer : More common in people between 30-50 years of age
Gastric ulcer : More common in
people beyond 60 years of age
Gender
Vol.04, Issue 01, January 2019 Available Online: www.ajeee.co.in/index.php/AJEEE
Duodenal ulcer : Occurs twice likely in men as compared to women
Gastric ulcer : More common in women
C. Ethnic Background
African-American or Hispanic backgrounds are more susceptible to develop PUD.
D. Other Risk Factors
People who have type O blood may have more chances to develop PUD, though it was previously thought to happen more in people who have type A blood (Wallace &
Granger, 1996).
General Representation of aggressive and defensive factors 1.4 Type of Peptic Ulcer
A. On the basis of location, peptic ulcer is categorized as follows:
a. Gastric Ulcer: Occurrence of ulcer in the stomach. It is more prevalent in old age people.
b. Duodenal Ulcer: Occurrence of ulcer in the duodenum. They occur more commonly in younger individuals, and it is evenly distributed among various socioeconomic groups. These patients have higher acid secretion rate than average level.
B. On the basis of severity, peptic ulcer is categorized as follows:
a. Acute Peptic Ulcer: These ulcers involve damage of tissues to the depth of the submucosa. They may arise in the form of single or multiple lesions. They are found in many sites of the stomach and the first few centimeters of the duodenum.
b. Chronic Peptic Ulcer: These ulcers penetrate through the epithelial and muscle layers of the stomach wall and may include the adjacent pancreas or liver. In the majority of cases, they occur singly in the pyloric antrum of the stomach and the duodenum.
1.5 Epidemiology of Peptic Ulcer
The time trends in epidemiology of peptic
ulcer disease show complex, multifactor
etiologies. Peptic ulcer was rare before the
1800s. The pathology of gastric ulcer
(GUs) was first described in 1835
(Cruveilhier J. Maladies de l'estomac et
al., 2012) during the late 1800s the
prominent form was GUs in young
women. Duodenal ulcer (DUs) was rare
until about 1900 and then became a
prevalent condition during the first half of
the 20th century. However, in developed
countries, the mortality from peptic ulcer
disease has fallen dramatically for birth
cohorts born after the 20th century.
Vol.04, Issue 01, January 2019 Available Online: www.ajeee.co.in/index.php/AJEEE
In particular, H. pylori was a prevalent
human infection well before the late 1800s, so that infection cannot explain the rise in ulcer prevalence and shift from GUs to DUs (Graham DY et al., 2012).
The influence of ecological factors on the pattern of gastritis may be a key variable in these birth-cohort effects. By the completion of the 19th century and currently in many developing countries H.
pylori infection was characterized by pan gastritis involving the gastric antrum and body and leading to acid hyposecretion, which predisposed to gastric cancer and GUs. (Graham DY et al., 2012). In contrast, DUs are associated with antral- predominant gastritis that spares the acid-secreting body but is negatively associated with more or severe body gastritis and with gastric cancer. (Valle J.
et al., 2012) The reason is that DUs require a permissive level of acid secretion which cannot be achieved in the face of moderate body gastritis, whereas gastric cancer is associated with hypochlorhydria.
2. LITERATURE REVIEW
Kohasu et al., (2015); evaluated the effect of Eriobotrya japonica seed extract (ESE) prepared with 70% ethanol on the gastric mucosal injury. Six experimental models with different action mechanisms were used for the evaluation. Three concentrations of ESE were prepared for each model. ESE administration was initiated 14 days before induction of gastric mucosal injury, and its effect was investigated. ESE inhibited the formation of gastric mucosal injury. Gastro protective activity of Eriobotrya japonica seed extract on experimentally induced gastric lesions in rats.
Kammoun et al., (2015); the study found the anti-inflammatory and the antioxidant activities of phenolic and flavonoids content in Eriobotrya japonica leaves. In the end, fractionation of EtOH/EtOAc 2:1 using CH2 Cl2/MeOh in different proportions was performed. The evaluation of these fractions shows that a correlation may exist between phenolic and flavonoids compounds and the anti- inflammatory and the anti-oxidant activities.
Bzeouich I et al., (2015); found that Eriobotrya japonica extracts showed neither mutagenic nor genotoxic effect.
The highest protective effect against
methyl methanesulfonate and 2- amino anthracene was obtained in the presence of aqueous extract, with IC50values of 80 and 140 µg/plate, respectively, against S.
Typhimurium TA104. Moreover, this extract (500 µg/plate) was also able to reduce significantly the genotoxicity induced by nitrofurantoin and aflatoxin B1 with IC50values of 140 and 240 µg/assay, respectively. Likewise, aqueous and TOF extracts inhibited xanthine oxidase and superoxide anion formation.
Khaled Nabih et al., (2014);
Investigated that the extract has significant antimicrobial activity, It inhibited significantly the development of Candida albicans suggesting that it can be used in the treatment of fungal infections. The extract has good antioxidant activity; it has revealed that high values of oxygen radical absorbance capability and Trolox equivalent antioxidant potential, while it presented a low value of polyphenol content. The phytochemical examination of the extract showed the presence carbohydrates, terpenes, tannins and flavonoids, further phytochemical analysis resulted in isolation and identification of three triterpenic acids, oleanolic, ursolic and corosolic acids and four flavonoids, naringenin, quercetin, kaempferol 3- O-β- glucoside and quercetin 3-O-α- rhamnoside.
Kim T-M et al., (2014); In this study, scientist evaluated the anti- asthmatic effects of EJ water extract in an ovalbumin (OVA) – induced BALB/c mice.
They also examined the activity of EJ in cell model for expression of nuclear factor kappa beta (NF-κB), extracellular signal- regulated kinases (pERK ½) in human tracheal smooth muscle cell (HTSMC) and inducible nitric oxide synthase ( iNOS ) and cyclooxygenase-2 (COX-2 ) in Raw 264.7 cell. Results suggest that allergic airway inflammation by inhibiting cytokine production, NO and also down- regulated the iNOs, COX-2, NF-kB &
pERK expression. E. japonica significantly decreases goblet cells hyperplasia inflammatory cells infiltration in OVA induced mice model.
Sharma K et al., (2011);
investigated that Eriobotrya japonica
leaves has been used traditionally to
reduce stress and anxiety. The study was
designed to evaluate the anti-anxiety
activity of various extracts viz. petroleum
Vol.04, Issue 01, January 2019 Available Online: www.ajeee.co.in/index.php/AJEEE
ether, toluene, ethyl acetate and methanol
of the leaves of using elevated plus maze (EPM) model in Swiss albino mice. Results showed that methanol and ethyl acetate extracts at the dose of 300mg/kg of the leaves of Eriobotrya japonica noticeably increased the average time spent in the open arms of the elevated plus maze. This effect was somewhat similar to the effect produced by diazepam.
Tierra, (2005); found E. japonica is rich in carotenoids, including provitamin A. The fruit and tender leaves are all used for medicinal purpose. The leaves and kernels contain amygdale in, which is known as an anti-cancer vitamin.
Jia W1 et al., (2003); the Chinese government has approved it as a blood- sugar supporter because it provides a set of natural bodily chemicals acknowledged as polysaccharides, compounds that have also been shown to increase insulin production.
Taniguchi S et al., (2002); stated that, out of all of its benefits, one of organic loquat’s impressive ability is that it may help in combating diabetes. Loquat leaf provides a variety of chemicals known as triterpenes. One of the most important acids is tormentic acid has been shown to increase insulin production which may help reduce the symptoms related to diabetes.
3. CONCLUSION
This paper related to number of researches for literature review, which will be help for profinding of results in research.
REFERENCES
1. McPherson, August F.P & Schweinfurth, August G., 1887. Illustration de la Flore d`Egypte 73, Photinia japonica.
2. Auria DD, Marinosci GZ, Benedictis GD and Piazza O., 2012. Vaptans and hyponatremia in critical patients.
Translational Medicine Vol. 3 Issue 1, pp.
1-14.
3. Avery JF., 1987. Prospects for peptic ulcer prevention. Postgrad. Med J; pp. 63: 233.
4. Biagioni M, Alpi A, Piccia relli P., 1990.
Aminopeptidases (EC.3.4.11) in alfalfa (Medicago sativa L.) leaves. J Plant Physiol, Vol. 135, pp. 559–564.
5. Brewster LM and Seedat YK., 2013. Why do hypertensive patients of African ancestry respond better to calcium blockers and diuretics than to ACE inhibitors and β- adrenergic blockers? A systematic review.
Biomed central Medicine. Vol. 11 Issue 141: pp 1-16.
6. Cruveilhier J. Maladies de l'estomac., 2012.
In: de l'Anatomie Pathologique du Corps Humain, Bailliere, Paris 1835.
7. De Tommasi, Nunziatina, Francesco De Simone, and Cosimo Pizza. (1992).
Constituents of Eriobotrya Japonica. A Study of Their Antiviral Properties. Journal of Natural Products Vol. 55: pp 1067-073.
8. Dharmani P, Kuchibhotla VK, Maurya R, Srivastava S, Sharma S, Palit G., 2004.
Evaluation of anti-ulcerogenic and ulcer healing properties of Ocimum sanctum Linn. J Ethnopharmacol; Vol. 93, pp 197- 206.
9. Ding CK, et al., 2001. Metabolism of phenolic compounds during loquat fruit development. J Agric Food Chem.
10. Editorial, 1996. Helicobacter pylori infection. Indian pediatrics; Vol. 33, pp 899-903.
11. Barar FSK., 2004. Essentials of Pharmacotherapeutics 8th Ed. New Delhi:
S Chand & Company Ltd, pp 536-537.
12. Barrett KE, Brooks HL, Boitano S and Barman SM., 2010. Renal function and micturition. In: Ganong’s Review of Medical Physiology 23th edition. New York, McGraw-Hill, pp 639
13. Ernst ME and Gordon JA., 2010. Diuretic therapy: key aspects in hypertension and renal disease. Public health and preventive nephrology, Vol. 23, Issue 5, pp 487-493.
14. Friedman PA and Berndt WO., 1997. Drugs affecting the cardiovascular system. In:
Craig CR and Stitzel RE (eds). Modern Pharmacology with ClinicalApplications 5th edition. Pp 239-254.
15. Garwood S., 2009. Osmotic Diuretics. In:
Ronco C, Bellomo R and Kellum JA (eds).
Critical Care Nephrology 2nd edition. New York, Elsevier.
16. Guyton AC, Hall JE., 2006. The body fluids and kidneys. In: Textbook of medical physiology 11th edition. Philadelphia, Elsevier, pp 325-359.
17. en.wikipedia.org/wiki/herbalism.
18. http://ntp.niehs.nih.gov
19. http://plants.usda.gov/java/profile?symbo l=acni2
20. http://www.crfg.org/pubs/ff/loquat.html 21. http://www.mdconsult.com/das/book/bod
y/1097055323/0/1249/181.html?tocnode
=5 1156474&fr omURL=181.html#4-u1.0- B0-7216-0187-1..50021-3--cesec80_2199) 22. Felker GM., 2012. Loop diuretics in heart
failure. Heart failure reviews, Vol. 17, Issue 2, pp 305-311.
23. Functional Foods in Health and Disease, 2012. Vol 2, Issue 3, pp. 48-61.
24. Ghaiye P., Sharma K., Kumar N., Niazi J., Gupta V., Bansal P., 2011. Anti- inflammatory & Antipyretic activity of Eriobotrya japonica leaves. Journal of Pharmacy Research, Vol. 4, Issue 4, pp 1147-1148
25. Godoy HT, Amaya DB., 1995. Carotenoid composition and vitamin A value of Brazilian loquat (Eriobotrya japonica Lindl.) . Arch Latinoam Nutr.
26. Graham DY., 2003. Changing patterns of peptic ulcer, gastroesophageal reflux disease, and Helicobacter pylori: a unifying hypothesis. Eur J Gastroenterol Hepatol;
Vol. 15, pp 571.
Vol.04, Issue 01, January 2019 Available Online: www.ajeee.co.in/index.php/AJEEE 27. Gupta M B, Vrat S, Nath R, Gupta G P,
Bhargava K P., 2012. Anti-ulcer of sodium valproate in rats and guinea pigs, Ind J Exp Bio, Vol. 26, pp 118-120.
28. Hamada, Atsuhide, Yoshioka S, Takuma D, Yokota J, Cui T, Kusunose M, Miyamura M, Kyotani S, and Nishioka Y., 2004. The Effect of Eriobotrya japonica Seed Extract on Oxidative Stress in Adriamycin-Induced Nephropathy in Rats. Biological and Pharmaceutical Bulletin. Vol. 27, pp 1961- 964.
29. Huang Y, Lu SJ, Dong JX, Li F., 2000. The new proof of neuroendocrine-immune network expression of islet amyloid polypeptide in plasma cells in the gastric mucosa of peptic ulcer patient. World J Gastroenterol, Vol. 6, Issue 3, pp 417-418.
30. Jackson K., 2006. Persistence of fixed versus free combination with valsartan and HCTZ for patients with hypertension. Value Health Suppl, Vol. 9, pp A363.
31. Jia, Wei, Gao W, and Tang L., 2003.
Antidiabetic Herbal Drugs Officially Approved in China. Phytotherapy Research, Vol. 17, pp 1127-134.
32. John LW, Li M., 2001. Inflammatory mediators in gastrointestinal defense and injury. Exp Bio Med, pp 1003-1015.
Journal of Natural Medicines., 2008.
(Impact Factor: 1.59), Vol. 62, Issue 1, pp 96-100.
33. Kim TM, Paudeln K.R., 1821. The Plant Resource Society of Korea Organization, Jeonju, South Korea Even Lindley, John.
Transactions of the Linnean Society of London, Vol. 13, Issue 1, pp 102.
34. Kammoun M, Ben A.Y, and Bezzine S., 2015. Antioxidant and Anti-inflammatory properties of Eriobotrya japonica leaves extracts. Journal of African Health Sciences: Makerere Medical School, Vol.
15, Issue 2, pp 613-620
35. Karakurt P, Kasikci M., 2012. Factors affecting prescription adherence in patients with hypertension. Vascular nursing Journal: official publication of the Society for Peripheral Vascular Nursing, Vol. 30, pp 118–26.
36. Khaled N.R, Butnariu M, 2014. Isolation and Antimicrobial and antioxidant Evaluation of Bio-active Compounds from Eriobotrya japonica Stems. Advanced Pharmaceutical Bulletin, Vol. 4, Issue 1, pp 75-81.
37. Kohasu, Oko-cho, Nankoku., 2015. Japan Science and Technology Agency, , Kochi, pp 783-8505.
38. Koti BC, Purnima A., 2008. Diuretic activity of extracts of Centratherum anthelminticum. International journal of green pharmacy, Vol. 2, pp 228- 231.
39. Lacy ER, Ito S., 1982. Microscopic analysis of ethanol damage to rat gastric mucosa after treatment with prostaglandin.
Gastroenterol, Vol. 83, pp 619.
40. Ljunghall S, Backman U, Danielson BG, et al. (1982). Effects of bendroflumethiazide on urate metabolism during treatment of patients with renal stones. J Urol, Vol. 127, pp 1207– 1210.
41. Mokdad-Bzeouich I, Kilani-Jaziri S, Mustapha N, Bedoui A, Ghedira K, Chekir- Ghedira L. 2015. Evaluation of the
antimutagenic, antigenotoxic, and antioxidant activities of Eriobotrya japonica leaves. Pharm Biol, Vol. 53, Issue 12, pp 1786-94.
42. Musini VM, Wright JM, Rezapour P, Bassett K and Jauca CD., 2012. Loop diuretics blood pressure lowering efficacy in primary hypertension (Review).
43. Nielsen S, Kwon TH, Christensen BM, Promeneur D, Frøkiær J and Marples D., 1999. Physiology and Pathophysiology of Renal Aquaporins. The American Society of Nephrology Journal Vol. 10, pp.647- 663.
44. Nishioka, Yutaka, Saburo Yoshioka, Masahiko K, Cui T, Atuhide Hamada, Masahide Ono, Mituhiko Miyamura, and Shojiro Kyotani., 2014. Effect of Extract Derived from Eriobotrya japonica on Liver Function Improvement in Rats. Biological and Pharmaceutical Bulletin, Vol. 25, pp 1053-057.
45. Okazaki M, Shimizu I, Ishikawa M, Fujiwara HY, Shiraishi T, Horie T, Luchi A, Ito S., 2007. Gastric mucosal levels of leukotrienes and prostaglandins in patients with the gastric ulcer after treatment with rabeprazole in comparison to treatment with ranitidine. J Med Invest. Vol. 54, pp 83-90.
46. Panda V. and Sonkamble M., Anti-ulcer activity of Ipomoea batatas tubers (sweet potato).Phyu Phyu Khine Zar. (1992). A Study of Their Antiviral Properties. Journal of Natural Products. Vol. 55, pp 1067-073.
47. Qui, B.S., Mei, Q.B., Liu, L. and Tchou- Wong, K.M., 2004. Effects of nitric oxide on gastric ulcers induced by nicotine and cold- restraint stress. World journal of gastroenterology, 10(4), p.594..
48. Rao Ch V., Vijayakumar M.., 2008. Effect of quercetin, flavonoids and tocopherol, an antioxidant vitamin on experimental reflux esophagitis in rats. Eur J Pharmacol, Vol 589, pp. 233-238.
49. Ruppert M, Overlack A, Kolloch R, et al., 1993. Neurohormonal and metabolic effects of severe and moderate salt restriction in nonobese normotensive adults. J Hypertens, Vol. 11, pp 743– 749.
50. Ryan MP, Ryan MF, Devane J, et al., 1984.
Effects of diuretics on renal handling of magnesium. Drugs, Vol. 28(suppl 1), pp 167–181.
51. Sachin SS, Archana RJ., 2009. Antiulcer Activity of Methanol Extracts of Erythrina indica Lam. Leaves in Experimental Animals. Phcog Res, Vol. 1, pp 396-401.
52. Shah SU, Anjum S and Littler WA., 2004.
Use of diuretics in cardiovascular disease:
hypertension. Postgraduate Medical Journal Vol. 80, pp 271-276.
53. Shah SU, Anjum S and Littler WA., 2004.
Use of diuretics in cardiovascular diseases:
(1) heart failure. Postgraduate Medical Journal, Vol. 80, Issue 8, pp 201-205.
Newjersy, John Wiley & Sons: 1-58.
54. Shchekochikhin D, Al Ammary F, Lindenfeld J and Schrier R., 2013. Role of Diuretics and Ultrafiltration in Congestive Heart Failure.Pharmaceuticals Vol. 6, pp 851-866.
55. Sharma K, Kumar N, Raj K, Niazi J, Gupta V., March 2011. Research Journal of Pharmaceutical, Biological and Chemical
Vol.04, Issue 01, January 2019 Available Online: www.ajeee.co.in/index.php/AJEEE Sciences (RJPBCS) Vol. 2, Issue 1, pp 255
ISSN: 0975-8585.
56. Snigdha M, Kumar SS, Jaya Y and Kasana B., 2013. A review on “how exactly diuretic drugs are working in our body.” Journal of Drug Delivery & Therapeutics, Vol. 3, Issue 5, pp 115-120.
57. Sood AR, Bajpai A, (1985). Digits M.
Pharmacological and biological studies on saponins. Indian J Pharmacol, Vol. 17, Issue 3. Pp 178-179.
58. Sundaram R & Murugesan g., 2011.
Hepatoprotective and antioxidant activity of mangrove plant Lumnitzera racemosa , Asian Pacific journal of tropical biomedicine., pp:384-352
59. Taniguchi, Shoko, Yokoi, Kobayashi E, Takamatsu Y, Ito H, Hatano T, Sakagami, Harukuni H, Tokuda H, Nishino, Sugita D, Shimura S, and Yoshida T., 2002.
Production of bioactive triterpenes by Eriobotrya japonica calli.Phytochemistry, Vol. 59: pp 315-23.
60. Tarnawski AS., 2005. Cellular and molecular mechanism of gastrointestinal ulcer healing. Digest Dis Sci, Vol. 50, pp 24-33.
61. Valle J, Kekki M, Sipponen P., 1996. Long- term course and consequences of Helicobacter pylori gastritis. Results of a
32-year follow-up study. Scand J Gastroenterol, Vol. 31, pp 546.
62. Wallace JL, Dicay M, McKnight W, Dudar GK., 2006. Platelets accelerate gastric ulcer healing through the presentation of vascular endothelial growth factor. British J Pharmacol Vol. 148, pp 274-278.
63. Wallace JL, Granger DN.,1996. The cellular and molecular basis of the gastric mucosal defense. FASEB J, Vol. 10, pp 731-740. 64.
Wilcox EB, Galloway LS., 1961. Serum and liver cholesterol total lipids and lipid phosphorus levels of rats under various dietary regimes. Am J Clin Nutr, Vol. 9, pp 236– 243.
64. Wilson DE., 2005. Therapeutic aspects of prostaglandins in the treatment of peptic ulcer disease. Dig Diseases and Sci. Vol.
31, Issue 2, pp 42-46.
65. Wright CI, Van-Buren L, Kroner CI and Koning MM., 2007. Herbal medicines as diuretics: a review of scientific evidence.
Journal of Ethnopharmacology, Vol. 114, Issue 1, pp 1-31.
66. Yancy CW, Bozkurt B, Jessup M, Butler J, Casey DE and Drazner MH et al. (2013).
ACCF/AHA Guidelines for Management of Heart Failure. Journal of the American College of Cardiology, Vol. 62, Issue 16, pp 147-239.