INTAKE OF SARDIN ELLA LONGICEPS OIL AS ANTI DISLIPIDEMIA THROUGH DECREASE OF LDL-C ON RAT WISTAR
Sri Wahjuni
Biochemistry Laboratory Chemistry Departement Faculty of Math and Science Udayana University
ABSTRACT
Nowadays fish consumption behaviour needs to be improved since the chandes of consumption paten to instant food. Fish, especially from deep see, is good for health, due to its rich content of polyunsaturated fatty acid (omega-3) which level is investigated in this research using true experimental study with randomized pre and posttest control group design. This research employed 50 Wistar rats which were divided into Sgroups, i.e.control group ()%SLO), treatment group l (10% SLO), treatment group 2 (15% SLO),treatment group 3 (20%SLO), and treatment group 4 (25%SLO). To obtain dislipidemia, the rats were fed with food rich in factor for 8 weeks, followed by determination of HDL level (pretest). After that, all rats were fed with sardinella longiceps oil for 6 weeks for dislipidemia and followed by determination of HDL.
Intake of 20% SLO resulted in an increase of blood LDL levels of dislipidemia Wistar rat about 22,78% from 55,97 + 5.l,25 to 68,73 +1,25 MG/dL. Further research regarding of whether the intake of SLO inhuman results in a similar effect to anti dislipidemia need to be carried out. Keywords: Fish consumption, antidislipidemia, sardinella longiceps
INTRODUCTION
Nowdays, fish consumption behaviour needs to be improve since the changes of consumption patern to instan food. Fish, especially from deep sea is good for health, due to the fish rich of polyunsaturated fatty acid (omega-3). Such fish including Thunnus Scombridae, Euthymrus sp, Scamberamorus, Decopterus, Rastrellinger, Sardinella Longiceps, Carangidae, Clupeidae, and Psettodeserumei. Sardinella Longiceps are a highly abundance fish found in Indonesian sea. Outbreak during peak season occures and as a consequence no economic value. Therefore, to increase their economic value, the fish can be managed to produce oil (Abdullah, 200; Ihsan, 2009).
Research on fish oil advantages to decrease dislipidemia have already widely carried out. This was intiated by the evidence that Japanese life longer compare to Mongolianese. This is as a results of Japanese have much more fish on their diet compare to meat consumption by Mongolianese. Fish consumption leads to lower of total cholesterol, LDL-cholesterol, and trigliceride and higher HDL cholesterol compare to meat consumption. This is because of fish contain much more polyunsaturated fatty acids omega-3 (Komatsu, et al., 2006; Fadilah, 2007).
to adhesion of thrombocyte to damaged and inflamated blood. Finally, results in contact of lower connected tissue to other elements in blood circulation. If; this damage goes chronically and ages, atherosclerosis process continually occurs and leads to thick tunica intima and disturbance of blood circulation on that site (Szmitko, et al., 2003).
Dyslipidemia is an abnormal lipoprotein metabolism, generally correlated to decrease or overproduction of lipoprotein. Dyslipidemia is frequently also known as hyperlipidemia associated with increase of lipid serum as a risk factor of cardiovascular disease. This is because of there is a cholesterol behavior which is play an important role on atherosclerosis in dyslipidemia. Therefore, differentiation between hypercholesterolemia with dyslipidemia is hypercholesterolemia is define as an increase of serum cholesterol more than 200 mg/Dl after 9-12 h starving. On the other hand, dyslipidemia define as the present of increase LDL-cholesterol serum more than 160 mg/D1, increase of triglyceride serum more than l50 mg/Dl or HDL-cholesterol below 40mg/Dl for man and below 50 mg/Dl for women, besides hypercholesterolemia criteria. High cholesterol symptom in dyslipidemia cannot be felt by dyslipidemia patients, however, this can only be known through routine check of blood cholesterol. High cholesterol diet and genetic induce dyslipidemia (Anonym, 2009).
Based on background explained above, the author want to investigate the effect of anti dislipidemia, through an decrease of LDL.
RESEARCH METHOD Research Design
This is a true experimental study with randomized pre and posttest control group design. This research employing 100 Wistar rats divided into two research, i.e. dislipidemia and atheroschlerosis. Each researchs applying 50 Wistar rat classified into 5 groups, i.e. control group (0% SLO), treatment group l (10% SLO), treatment group 2 (15% SLG), treatment group 3 (20% SLO), and treatment group 4 (25% SLO).
Initial step is to prepaired all rats in similar condition, therefore, all rat were feeded with ITB diet for 4 weeks. Then to obtain dislipidemiarat (Research I), rats were fed with food rich of fat (UNAIR diet) for 8 weeks, followed by determination LDL-C levels (pretest data).
Location And Time Schedule
Rats preparation were carried out at Center Study of Animal Diseases(CSAD)Veterinary Faculty Udayana University.LDL-C determination was carried out at UPT. Laboratorium Analitik Universitas Udayana. Research was carried out for 12 months including data analysis and writing the results.
Data Analysis
All data were analyzed descriptively. Mean difference decrease of decrease of LDL-C were analyzed using anova one way at 5% significant levels.
RESULTS
Decrease of LDL-C levels of dislipidemia Wistar rat
Mean decrease data of LDL-C of dislipidemia Wistar rats for pre and posttest were listed on Table 1. The data on Table l were normally distributed and their variance were also homogeneous insicates by p > 0.05. Mean different profile of LDL-C levels after treatment of various SLO intake was presented on
Decrease of LDL-C levels of dislipidemia Wistar rat
Mean LDL-C levels of Wistar rat pretest and postest data were listed on Table l.
Table l Decrease of LDL-C Levels
Data on Table 1 are normaly distributed and their variance also homogeneous with p> 0 05 Mean profile different of LDL-C difference of various SLO intake was presented in Figure 1
Figure 1
Mean Different Profile of LDL-C Difference for Posttest
Anova test indicates that there is a significant different of SLO various intake with p< 0 05 Resume of the test was presented on Table 2.
DISCUSSION
Dyslipidemia
A number of 50 Wistar rat for dislipidemia have already investigated. Dislipidemia research was applied by feeding of high fat diet (UNAIR diet) for 8 weeks, compare to 13 weeks for atheroschlerotic research. Mean weight of initial Wistar rat is 49.78 dc 0.77) g. After the present of dislipidemia, the mean weight is about 201.75 ± 0.51 g (pretest data). Mean weight of Wistar rat alter intake of various SLO for 6 weeks is 203.78 ± 1.03 g (posttest data).
Decrease of LDL-C blood levels of dyslipidemia Wistar rat
In this research, it was obtained that intake of various SLO concentration decrease blood LDL-C levels of dyslipidemia Wistar rat. Mean LDL-C blood levels of dyslipidemia Wistar rat were presented on Table 1. Mean HDL-C blood levels of dyslipidemia Wistar rat for pretest with intake of 0%, 10%, 15%, 20%, and 25% SLO were kolest-LDL pre danposttest (144,05;t0,02) and (l41,06 :l:l,54) mg/dL, respectively. The mixture of MIL 10% results in the levels of kolest-LDL pre and posttest (144,09 ± 0,08) and (140,99±1,38) mg/dL. The table also showd the level of kolest-LDL for MIL 15%, 20% dan 25% pre and posttest (144,05±0,08) and (134,52i1,89) mg/dL; (l44,08±0,02) and (126,12±1,61) mg/dL; (144,08±0,03) and (134,52±3,51) mg/dL respectively. This research shows that lowering of the levels of kolest-LDL took place at all treatments (Figure 5.3). From the same table, it can also be seen that mean HDL-C blood levels of dyslipidemia Wistar rat for posttest with intake of 0%, 10%, 15%, 20%, and 25% SLO were (56.84 ± 1.25); (58.14 ± 1.38); (59.26 ± 0.84); and (68.72 ± 0.86) mg/dL, respectively. The increase different of HDL-C blood levels of dislipidemia Wistar rat caused by intake of 0%, 10%, 15%, 20%, and 25% SLO can be seen on Table 4.10. This table reveals that the highest increase of 11.88 mg/dL HDL-C blood levels of dislipidemia Wistar rat was observed for intake of 20% SLO, compare to 1.30 mg/dL for intake of 10% SLO, and 2.72 mg/dL for intake of 15% SLO. These were compared towards HDL-C blood levels of dislipidemia Wistar rat with intake of 0% SLO. An interesting trend observed in this research was increase of 2.54 mg/dL HDL-C blood levels of dilipidemia rat due to intake of 25% SLO, as indicated by Figure 4.5. However, that increase is not as big as for intake of 20% SLO about 11.88 mg/dL. These trends occure in all treatments of SLO intake, including decrease of LDL-C and MDA blood leves.
In dyslipidemia case, cell membrane was saturated of cholesterol due to exessive of LDL acceptance and endogenebiosintesys. To overcome this situation, naturaly cholesterol balancing occures trough pick cholesterol up and distributed to extracelular Hood and return it to liver. This event known as reverse cholesterol transport and was carried out by HDL as an antithrombin (Devlin, 1986; Murray, 2004). Possible mechanism is due to anti oxidant inactivation, that function to break down unsaturated fatty acids. Long and continue exposure induce leucocyte adhesion to vascular endotel which leads to endotel cells promote cholesterol effux that have as role to control vascular (Tatong, 2003). This is conform to hypothesis 5, i.e intake of SLO increase HDL-C blood levels of dislipidemia Wistar rat.
CONCLUSION
It can be concluded that:
1. Intake of 20% SLO results in increase of LDL-C blood levels of dislipidemia Wistar rat about 22.78%, from 55.97i1.25 to 68.73 il.25 mg/dL; and
REFERENCES
Abbas, K. A., Lichtman, A. H., and Pober, J _ S. 2000. Cytokin in Cellular and Moleculer Immunology 4th ed. Philadelphia, WB Saunders; 233-267.
Abdullah-Rasyid. 2001. Prosiding Seminar IPT EK Kelautan Nasional, Pusat Penelitian Oseanografi LIPI Jakarta.
Ahmed, E. 2001. Immune Mechanism in Atherosclerosis. Dissertation. ISSBN: 91-628-4612-4. Konferensrummet, Centrum for Molekular Medicin, Karolinska Sjukhuset.
Ahmed, M. S., and Olfat, M. Y. 2010. Physiological Studies on the Risk Factors Responsible for Atherosclerosis in Rats. Nature and Science. 8(5); 144-155.
Anonim. 2009. Health: Hypercholesterolemia. College of Medicine. Milton State Hershey Medical Center Penn State. America.
Anonim. 2007. Minyak Ikan Berkhasiat Turunkan Serangam Jantung. Depot ikan Jakarta: Serpong. Fadilah, S. 2007. Pengaruh diit minyak ikan lemuru terhadap kaclar lnoid plasma dan agregasi
platelet pada orang sehat. Journal colletion departemen kardiologi dan kedokteran vaskuler Universitas Indonesia.
Gatot, S. L. 2005. Sindrom Metabolik Merupakan Manisfestasi dari Keadaan Inflamasi. Jurnal Medicin. 26 (1). Universitas Hasanudin Makasar.
Murray, K. 2004. Harper Biochemestry twenty sixth edition. Mc Graw Hill Companie; New York. Pramesti, G. 2007. Aplikasi SPSS 15.0 dalam Model Linier Statistika. Jakarta: Penerbit PT Elex
Media Komputindo.
Szmitko, P. E., Wang, C. H., Weisel, R. D., De-Almmeida, J. R., Anderson, T. J., and Verma, S. 2003. New Markers of Inflamamtion and Endothelial Cell Activation. Circulation 108: 1917-1923.
Tatong, H. 2003. Fungsi Endotel dan pengaruhnya pada berbagai gangguan fungsi kardiovaskuler. Malang Press. Fakultas Kedokteran Universitas Brawijaya.
