Antihyperlipidemic Activity of Cucumis Melo

International Journal of Universal Pharmacy and Bio Sciences 1(1): September-October 2012
INTERNATIONAL JOURNAL OF UNIVERSAL PHARMACY AND BIO SCIENCES

Pharmaceutical Sciences
Research Article!!!
Received: 05-10-2012; Accepted: 12-10-2012 ANTI-HYPERLIPIDEMIC ACTIVITY OF CUCUMIS MELO FRUIT PEEL
DIFFERENT EXTRACT IN TRITON X-100 INDUCED HYPERLIPIDEMIA IN RATS Jayant S. Bidkar *, Madhuri D. Bhujbal , Ganesh Y. Dama Department of Pharmacognosy, Sharadchandra Pawar College of Pharmacy, Dumberwadi (Otur), Tal.Junner, Dist.Pune, 410504, Maharashtra, India.
KEYWORDS: Antihyperlipidemic activity, Triton induced hyperlipidemia, Cucumis melo fruits peel. For Correspondence: Mr. Jayant S. Bidkar, Department of Pharmacognosy, Sharadchandra Pawar College of Pharmacy, Dumberwadi (Otur), Pune, 410504. E-mail:
jayantbidkar@yahoo.com
ABSTRACT Cucumis melo Linn. (Cucurbitaceae) fruits have been used, traditionally, for the treatment of various disorders of heart as Cardioprotective and antiobesity. The aim of the present study was to investigate the possible anti-hyperlipidemic activity of Cucumis melo fruit peel extract in triton induced hyperlipidemia in rats. Chloroform, Methanolic and aqueous extracts of were administered to the triton induced hyperlipidemic rats for 7 days to study antihyperlipidemic acivity. The acute toxicity value of chloroform, methanol and aqueous extract after oral administration in mice were found to be 5000 mg/kg. The results concluded that CMFP methanolic extract (500 in mg/kg) Triton have X-100 definite induced
antihyperlipidemic
activity
hyperlipidemia model and which is equipotent activity when compared with Atorvastatin treated group.
Full Text Available On www.ijupbs.com
1. INTRODUCTION Current predictions estimate that by the year 2020 cardiovascular diseases, notably atherosclerosis, will become the leading global cause of total disease burden, defined as the years subtracted from healthy life by disability or premature death an important factor in causing atherosclerosis is hyperlipidemia [1]. Hyperlipidemia is the presence of raised or abnormal levels of lipids and/or lipoproteins in the blood [2]. It is also called hyperlipoproteinemia because these fatty substances travel in the blood, attached to proteins and this is the only way that these fatty substances can remain dissolved while in circulation. It is also synonymously known as dyslipidemia [3]. The randomly collected data clearly demonstrated that some forms of dyslipidemias were very common in adults all over the world. During the past decade, a vast amount of evidence has confirmed the critical role played by the dyslipidemias in the pathogenesis of atherosclerosis, coronary artery disease etc [4]. The advantages of lowering lipid levels to satisfactory levels have been confirmed by several experimental and interventional studies indicating lower morbidity and mortality in coronary heart disease which commensurate with reduction of serum cholesterol [5]. Cucumis melo Linn (Syn. Cucumis callosus (Rottl.) Cogn. Cucumis trigonus Roxb. Family Cucurbitaceae) popularly known as Muskmelon [6]. Cucumis melo Linn (CM) is a pubescent or trailing herb with edible, polymorphous fruits. It is used for various ailments in Indian Traditional System of Medicine. Fruit and roots have medicinal value. The fruits are used in flatulence, leprosy, fever, jaundice, diabetes, antiobesity, cough, bronchitis, ascites, anaemia, constipation, other abdominal disorders and amentia [6, 7, 8]. In addition, fruit pulp is bitter, acrid, thermogenic, anthelmintic, liver tonic, cardio tonic, appetizer, expectorant and intellect promoting. Roots are used as emetic and purgative [7]. Earlier works on CM fruits showed effectiveness in preventing chemically induced hypothyroidism in rats [9]. Some other research studies are available on its urease inhibitory, antioxidant, antiinflammatory, antiulcer and diuretic [10, 11, 12]. Phytochemical investigations revealed the presence of phenolic glycoside(E)-4-hydroxycinnmyl benzyl alcohol 4-O-(2'-O--D3,29-O -D-glycopyranoside, O--Dglucopyranoside,
apiofuranosyl)(1"2')-
dibenzoylmultiflor-8-en-3,7,29-triol and 3-O-p-amino-benzoyl-29-O benzoylmultiflor-8-en-3 , 7,29-triol was isolated and identified from Cucumis melo seeds [13].
CM fruits are used traditionally in Indian traditional system of medicine, and also various uses have been described including for obesity [8] but there is no much scientific study reported about antihyperlipidemic activity. Therefore present study was undertaken to establish the acute toxicity study and scientifically evaluate the antihyperlipidemic activity of the Chloroform, methanol and aqueous extracts of CM fruits peel (CMFP) in Triton X100 induced hyperlipidemia model in Wistar rats. 2. MATERIALS AND METHODS 2.1 Plant material: The fresh trailing herb with fruits of C.melo Linn was collected from Pune district (M.S.) in the months of July-August. The trailing herb was authenticated by Mr. P. G. Diwakar, Deputy Director, Botanical Survey of India, Pune through comparing morphological features. The herbarium of the plant specimen was deposited at Botanical Survey of India. Voucher specimen number DDG-4 (Ref. No.BSI/WRC/Tech/2010/428 dated 09.09.2010). They were peeled off mechanically and good quality peels were air dried under shadow and then grounded into coarsely powdered in grinder and powder material was passed through 120 mesh to remove fine powders and coarse powder was used for extraction. 2.2 Protocol for Successive Extraction The coarse powder of CMFP (100 gm) was extracted by using successive soxhlet extraction using solvents of varying polarity such as petroleum ether (60-80c), chloroform, methanol, distilled water (8.2, 10.1, 4.2, 8.5g respectively) for 72 hrs. After completion of extraction, solvent was distilled off and concentrated extract was air-dried [14]. Petroleum ether extraction was used defatting. Chloroform, Methanol, Aqueous extract was mixed with 5% CMC and which was used for the antihyperlipidemic activity. 2.3 Phytochemical screening: The crude extract obtained by using various solvents were analyzed for alkaloids, tannins, saponins, steroids, flavonoids, and phenolic compound using standard procedure of analysis [15].
2.4 Chemicals Triton was purchased from Merck Limited, Mumbai, India. Cholesterol kit (Enzymatic Method), HDL-C kit, Triglycerides were procured from Beacon Diagnostics PVT.LTD, Navasari, India. All solvents used for extraction procured from Merck Limited, Mumbai, India. 2.5 Animal Wistar albino male rats weighing 200-220g and albino mice (Either sex) weighing 20-25g were selected and housed in polypropylene cages in a room where the congenial temperature was 27C 1C and 12 hrs light and dark cycles were maintained. The animals were allowed to acclimatize to the environment for 7 days and supplied with a standard pellet diet (VRK nutritional solution, Pune) and water ad libitum. 2.6 Acute toxicity study Albino mice (Either sex) of 10 animals per group and weighing 20-25 g were administered graded dose (100-5000 mg/kg body weight, p.o.) of the chloroform, methanolic and aqueous extracts of CMFP. After administration of the extract the mice were observed for toxic effects for 48 hr. The toxicological effects were observed in terms of mortality expressed as LD50. The number of animals dying during a period was noted. The LD50 of the extract was determined by Litchfield and Wilcoxon (Litchfield and Wilcoxon, 1949) method [16]. 2.7 Anti-hyperlipidemic activity Hyperlipidemia was induced in Wistar albino male rats by single intraperitoneal injection of freshly prepared solution of Triton-X-100 (100 mg/kg) in physiological saline after overnight fasting for 18 hours [17, 18]. The rats were divided into nine groups of six rats in each group and were treated with single dose/day (p.o.) of standard drug or extracts of CMFP. The first group was given Standard pellet diet, 5% CMC, and water (Served as normal control). The second group was given a single dose of triton at a dose 100 mg/kg, i.p. After 72 hours of triton injection, this group received a daily dose of 5 % CMC (p.o.), for 7 days (Served as Triton control). The third to eight group was administered a daily dose of CMFP Chloroform, Methanol and aqueous extract at a dose 250 mg/kg and 500 mg/kg suspended in 5% CMC, p.o. (served as treatment groups) for seven days, after inducing hyperlipidemia. Ninth group was administered with
Standard Atorvastatin 10 mg/kg p.o. for 7 days (served as standard). 2.8 Collection of blood samples On 8th day of treatment, the blood was collected by retro orbital sinus puncture, under mild ether anesthesia in plane tubes. Serum obtained by immediate centrifugation of blood samples using remi ultra cooling centrifuge at 3000 rpm for 5 minutes at room temperature and was directly used for estimating serum lipid profiles (serum TC, TG, LDL-C and HDLC). All samples were stored at 4C until analysis. 2.9 Biochemical analysis Serum lipid levels include TC, TG and HDL-C, were carried out using respective
diagnostic commercial kits from Qualigens diagnostics, Mumbai, India and LDL-C in plasma was calculated as per friedewald estimation [19], LDL-C= (TC-(TG/5+HDL)-C) mg/dl, VLDL=(TG/5), Atherogenic Index=TC/HDL-C. 2.10 Statistical analysis The results were expressed as mean SD. The Triton control was compared with normal and the experimental results were compared with Triton control. Statistical analysis was carried out using paired t-test and one-way ANOVA followed by Dunnett test. Differences below P<0.05 implied statistically significance. 3. RESULTS 3.1 Phytochemical screening The results of phytochemical screening in table 1. indicated the presence of maximum amount of steroids and Steroidal glycosides, in Chloroform extract., Carbohydrate, Flavonoids, Tannins, Saponins, steroids are present in Methanolic extract and Aqueous extract contains Carbohydrate, Flavonoids, Saponin and Tannins. 3.2 Acute toxicity study The acute toxicity studies of chloroform, methanolic and aqueous extract of the CMFP were found to be non-toxic up to the dose 5000 mg/kg and did not show any mortality.
3.3 Anti-hyperlipidemic activity The systemic administration of the surfactant Triton to fasted or non-fasted rats results in the elevation of plasma cholesterol and triglyceride levels. The dyslipidemia of the metabolic syndrome consists of hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol, and a higher proportion of small, dense low-density lipoprotein (LDL) particles. An increased risk of coronary heart disease is associated with a high serum concentration of total cholesterol, LDL and triglyceride [20]. The results of present study are given in Table 2-3. The rats treated with triton showed significant increase in serum cholesterol level from 54.08 mg/dl in normal rats to 137.53 mg/dl, triglyceride level from 59.53 mg/dl in normal rats to 111.51 mg/dl and LDL-C from 20.24 mg/dl in normal rats to 86.02 mg/dl. Treatment with CMFP different extract at the different doses of 250 mg/kg, and 500 mg/kg reduced the serum TC, TG & LDL-C levels & increased the serum HDL-C levels when compared to the hyperlipidemic control group. It is widely accepted that reduction in plasma HDL-C level is a risk factor for developing atherosclerosis [21]. The change in lipid levels in group number III-VIII, were comparable with group of Atorvastatin treated rats. Methanolic and aqueous extract showed a dose dependant decrease in the levels of cholesterol, Triglyceride, and LDL-C level. Among five groups (i.e. group number III-VIII), group number VI reduced the elevated lipid levels more significantly than the others while CMFP chloroform extract having very low hypolipidemic activity. Administration of methanolic extract of CMFP at a dose of 500 mg/kg and standard drug 10 mg/kg the cholesterol level is 60.13 mg/dl triglyceride level is 68.63 mg/dl and HDL-C level is 25.57 mg/dl as compare to standard drug Atorvastatin where decrease of cholesterol level is by 58.17 mg/dl triglyceride level is by 61.92 mg/dl and HDL-C level is 26.70 in triton induced hyperlipidemic rats. A significant increase in HDL-C which was related to a significant reduction of atherogenic index was observed (8.01 to 2.17). 4. DISCUSSION Hyperlipidemia is widely known to be the major risk factor for the development of cardiovascular diseases. Coronary heart diseases, stroke, atherosclerosis and hyperlipidemia are the primary cause of death [22-23]. Therefore, prime consideration in the therapy for hyperlipidemia and arteriosclerosis is to attenuate the elevated blood serum/plasma levels of lipids. The currently availa-
-ble antihyperlipidemic therapy includes mainly HMG-CoA reductase inhibitors (Statins), Bile acid sequesterants (Resins), Activate lipoprotein lipase (Fibric acid derivatives), Inhibit triglyceride synthesis (Nicotinic acid) and others (Gugulipid, Ezetimibe, Policosanol) [26]. Though there are a large number of antihyperlipidemic agents used in the treatment, none of the existing one available worldwide are fully effective, absolutely safe and free from side effects [25]. So efforts are being made to find out safe and effective agents that may be beneficial in correcting the lipid metabolism and preventing cardiac diseases. Many herbs and plant products have been shown to have antihyperglycaemic and antihyperlipidemic properties [26]. Cucumis melo is a drug-plant used traditionally for the treatment of heart disorders as Cardioprotective. The purpose of this work was to evaluate the traditional claims of Cucumis melo on scientific basis in experimentally induced hyperlipidemia. Single administration of CMFP diffrent extract in various doses (100-5000 mg/kg) did not show any mortality, this indicate the extracts safety and absence of toxicity in the doses studied. The results of our present study clearly indicate that CMFP methanolic and aqueous extract at a dose of 250 and 500 mg/kg significantly lowered serum cholesterol and triglyceride levels i.e. antihyperlipidemic activity which was found to be more effective in higher dose as compared to lower dose when administered orally in triton induced hyperlipidemic models. The serum cholesterol lowering effect of CMFP methanolic and aqueous extract may be due to the inhibition of cholesterol biosynthesis. The methanolic and aqueous extract of CMFP decreased the serum triglyceride level may be due to increased catabolism of triglyceride and an inhibition of fatty acetyl-CoA activity and glycerophosphate acetyl transferase. The HDL-C level is inversely related to total body cholesterol and reduction of plasma HDL concentration may accelerate the development of atherosclerosis, leading to ischaemic heart disease, by impairing the clearance of cholesterol from the arterial wall [27]. (References, Miller and Miller) In the CMFP methanolic and aqueous extract treated groups of animals showed slightly increase the serum HDL-C levels in triton induced hyperlipidemic model. The increase in HDL-C level may be due to the activity of LCAT and inhibition of the action of hepatic TG-lipase on HDL, which may contribute for rapid catabolism of blood lipids through extra hepatic tissues.
Total cholesterol / HDL-C ratio of > 4.5 is associated with increased coronary heart disease risk and the ideal ratio is 3.5 [28]. A significant decrease in the atherogenic index on CMFP methanolic and aqueous extract treatment shows that the protective efficacy of the extract against atherogenesis. Preliminary phytochemical screening revealed the presence of flavonoids, tannins, steroids and steroidal glycosides in CMFP methanolic and aqueous extract. It is found that some saponins increase the permeability of mucosal cells in vitro, inhibit active mucosal transport and facilitate uptake of substances that are normally not absorbed [29]. Phytosterols are reported to displace intestinal cholesterol and reduce cholesterol absorption from intestine. Flavonoids have exhibited a variety of pharmacological activities, including the antiatherogenesis and antioxidant effect [30]. Thus the present result strongly suggests that the hypolipidemic activity of this medicinal plant could be attributed to the presence of saponins, steroids and flavonoids in the extract. CONCLUSION: The results concluded that CMFP methanolic extract (500 mg/kg) have definite antihyperlipidemic activity in Triton X-100 induced hyperlipidemia model and which is equipotent activity when compared with Atorvastatin treated groups. Further studies on this extract may lead to identify the possible mechanism of action and isolation of active principle from the same. REFERENCES: 1. Kaur SC, (2006); Advances in biochemistry in health and disease., Biochemistry of Atherosclerosis 16, p. 572. 2. Frederickson DS, Lee RS, (1965), A system for phenotyping hyperlipidemia. Circulation 31, p. 321-327. 3. Chen H, (2005), Hyperlipidemia Health Encyclopedia-Diseases and Conditions., [Online].Available at: http://www.merck.com/mmpe/sec12/ch159/ch159b.html.
4. Vega GL, Sirtori C, (1996), Dyslipidemia and coronary heart disease, Current Opinion in Lipidology, 7, p. 179-82. 5. Jackson R, Beagle HR, (1995), Evidence-based management of dyslipidemia, Lancet, 346, 1440-44. 6. Asima Chatterjee, satyesh Chandra Prakrashi, (1997), The treatise on Indian medicinal plants, Vol 5, National institute of science and information resources, New Delhi, p. 114-16. 7. Kirtikar KR, Basu BD, (1984), Indian medicinal plants, M/S Periodical Experts, New Delhi, p. 1585-88. 8. Vijayvergia VA, (1999), Coughcide kachri. Rajasthan Patrika, Jaipur Issue,
Available at: www.actahort.org/members/showpdf?booknrarnr=752_30. 9. Hamendra Singh Parmar, Anand K, (2009), Protective role of Mangifera indica, Cucumis melo and Citrullus vulgaris peel extracts in chemically induced hypothyroidisma, Chemico-Biological Interactions, 177, p. 254258. 10. Malhotra OP, Rani I, (1978),Occurrence, isolation & characterization of urease inhibitor from melon (Cucumis melo) seeds, Ind. J. Biochem. Biophysics,15, 229231. 11. Vouldoukis I, Lacan D, Kamate C, Coste P, Calenda A, Mazier D, Conti M, Dugas B, (2004), Antioxidant and anti-inflammatory properties of a Cucumis melo LC. extract rich in superoxide dismutase activity, Journal of Ethnopharmacology,94, p.6775. 12. Singh RC, Sisodia CS, (1970), Pharmacodynamic investigations into the diuretic activity of Cucumis melo seed (ether extract), Ind. J. Med. Res., 58, p. 50512. 13. Simona De Marino, Carmen Festa, Franco Zollo, Maria Iorizzi, (2009), Phenolic glycosides from Cucumis melo var. inodorus seed, Phytochemistry Letter 2, p.13033. 14. Mukharjee PK, (2002), Quality Control of Herbal Drug, first ed., Business Horizon Publication, New Delhi, p. 405-06. 15. Kokate CK, (1996), Practical Pharmacognosy, 4th ed.Vallabh Prakashan,Pune, p.107. 16. Litchfield JT, Jr. and Wilcoxon F, (1949), A simplified method of evaluating dose effect, J. Pharmac.exp. Ther, vol. 96, no. 2, p. 99-113. 17. Mohale DS, Dewani AP, Saoji AN, Khadse CD,(2008), Antihyperlipidemic activity of isolated constituents from the fruits of Lagenaria siceraria in albino rats. I.J. of G. P., p. 104-07.
18. Ansarullah RN, Jadeja MC, Patel TV, Ramachandran AV, (2009), Antihyperlipidemic potential of a polyherbal preparation on Triton WR 1339. (Tyloxapol) induced hyperlipimia: A comparison with Lovastatin, International Journal of Green Pharmacy, p. 119-24. 19. Friedewald WT, Levy RI, Friedrickson DS, (1972), In: Tietz (Ed) Determination of LDL cholesterol, Text Book of clinical Biochemistry, New York, p.874-98. 20. Sheehan MT, Jensen MD, (2000), Metabolic Complications of Obesity, Medical Clinics of North America, 84(20) p. 363-85. 21. Gordon DJ, Probstifield JL, Garrision RJ, Neaton JD, Castelli WP, Knoke JD, Jacobs Jr., DR, Bangdiwala S and Tyroler HA, (1989), High density lipoprotein cholesterol and cardiovascular disease, four prospective American studies, Circulation, 79, p. 8-15. 22. Grundy SM, (1986), Cholesterol and coronary heart disease a new era: Journal of American Medicine, 256 p. 2849-2858. 23. Davey Smith G, (1993), Cholesterol lowering and mortality the importance of considering initial level of risk: International journal of medicine, 306, 1367-1373. 24. Havel R, Rapaport E, (1995), Management of primary Hyperlipidemia, N.E.J.M, 332:14918. 25. Ghatak A, Asthana OP, (1995) Recent trends in hyperlipoproteinemias and its pharmacotherapy, Indian journal of Pharmacology, 27, 14-29. 26. Brown GB, Xue-Qiao, Sacco DE, Alberts JJ, (1993), Lipid lowering and plaque regression, New insights into prevention of plaque disruption and clinical events in coronary disease, Circulation, 87, 1781-91. 27. Kanungo SK, Panda DS, Swain SR, Barik BB, and Tripathi DK, (2007), Comparative evaluation of hypolipidemic activity of some marketed herbal formulation in triton induced hyperlipidemic rats Pharmacologyonline, 3, 211-21. 28. Castelli WP, Garrison RJ Wilson PWF, Abbott RD, Kalousdian S and Kannel WB, (1986), Incidence of coronary heart disease and lipoprotein cholesterol levels-The Firmingham Study, JAMA, 256, 2835. 29. Johnson IT, Gee JM, Price KR, Curl C and Fenwick JR, (1986), Influence of saponins on gut permeability and active nutrient transport in vitro. J. of Nutrition, 116, 2270-77. 30. Bangham AD and Home RW, (1962), Action of saponins on biological membranes, Nature, 196, p. 952-953.
10
Table 1: Phytochemical screening of CMFP different extracts Chemical constituents Chloroform extract Carbohydrates Tannins Alkaloids Saponins Flavonoids Glycosides Steroids Amino acids Proteins + + ++ Methanolic extract ++ ++ ++ + + ++ + + Aqueous extract ++ ++ ++ + + + +
+: Presence of Chemical constituents, -: Absence of Chemical constituents, ++: Maximum presence of Chemical constituents.
Full Text Available On www.ijupbs.com 11
Table 2. Effect of CMFP various extract on TC, TG and VLDL-C level in Serum of control and experimental Rats. Groups Parameters Total Cholesterol Triglyceride Group-I Normal control Group-II Triton control 54.082.67 137.532.77## 59.532.65 111.513.09## VLDL-C 12.000.54 22.300.62## 18.500.41**
Group-III Triton + CMFP Chloroform 112.902.869** 92.482.02** extract 250 mg/kg Group-IV Triton + CMFP Chloroform 95.988.80** extract 500 mg/kg Group-V Triton + CMFP Methanolic 75.383.57** extract 250 mg/kg Group-VI Triton + CMFP Methanolic 60.132.84** extract 500 mg/kg Group-VII Triton + CMFP Aqueous 250 81.252.59** extract mg/kg Group-VIII Triton + CMFP Aqueous 500 66.372.14** extract mg/kg Group-IX Triton + Atorvastatin 10 mg/kg 58.173.06** 61.921.38** 70.452.20** 86.682.66** 68.632.83** 76.602.28** 81.853.88**
16.370.78**
15.320.46**
13.730.57**
17.330.53**
14.090.44**
12.380.28**
Values are expressed as meanS.E.M (n=6); ##P< 0.01 when compared with Group I (Normal control); **P<0.01 when compared with group II (Triton control).
Full Text Available On www.ijupbs.com 12
Table 3. Effect of CMFP various extract on LDL-C, HDL-C level and Atherogenic index in serum of control and experimental Rats. Groups Parameters HDL-C LDL-C Atherogenic Index Group-I Normal control Group-II Triton control 21.850.63 17.270.56## 20.242.41 86.022.383## 72.193.292** 2.470.16 8.010.35## 5.160.35**
Group-III Triton +CMFP Chloroform 22.181.13** extract 250 mg/kg Group-IV Triton + CMFP Chloroform 23.221.08** extract 500 mg/kg
56.558.31**
4.1830.43**
Group-V Triton + CMFP Methanolic 25.350.650** 34.713.79** extract 250 mg/kg Group-VI Triton + CMFP Methanolic 25.571.23** extract 500 mg/kg Group-VII Triton + CMFP Aqueous 25.020.61** extract 250 mg/kg Group-VIII Triton + CMFP Aqueous 25.351.02** extract 500 mg/kg Group-IX Triton +Atorvastatin 10 mg/kg 26.700.77** 19.082.19** 26.911.03** 39.161.85** 20.841.35**
2.990.22**
2.350.05**
3.270.08**
2.620.07**
2.170.06**
Values are expressed as meanS.E.M (n=6); ##P< 0.01 when compared with Group I (Normal control); **P<0.01 when compared with group II (Triton control); ns P>0.05, non significant when compared with group II (Triton control). Full Text Available On www.ijupbs.com 13

Antihyperlipidemic Activity of Cucumis Melo

Diunggah oleh

Informasi Dokumen

Deskripsi Asli:

Judul Asli

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Antihyperlipidemic Activity of Cucumis Melo

Diunggah oleh

Hak Cipta:

Format Tersedia

International Journal of Universal Pharmacy and Bio Sciences 1(1): September-October 2012

INTERNATIONAL JOURNAL OF UNIVERSAL PHARMACY AND BIO SCIENCES

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com

Full Text Available On www.ijupbs.com 11

Full Text Available On www.ijupbs.com 12

Anda mungkin juga menyukai