{"id":53046,"date":"2023-12-31T10:54:36","date_gmt":"2023-12-31T10:54:36","guid":{"rendered":"https:\/\/biomedpharmajournal.org\/?p=53046"},"modified":"2024-01-05T06:41:39","modified_gmt":"2024-01-05T06:41:39","slug":"protective-effect-of-ethanolic-extracts-of-syzygium-campanulatum-leaf-in-wistar-albino-rats-against-triton-and-atherogenic-diet-induced-hyperlipidemia","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol16no4\/protective-effect-of-ethanolic-extracts-of-syzygium-campanulatum-leaf-in-wistar-albino-rats-against-triton-and-atherogenic-diet-induced-hyperlipidemia\/","title":{"rendered":"Protective effect of Ethanolic Extracts of Syzygium Campanulatum leaf in Wistar Albino Rats Against Triton and Atherogenic Diet-Induced Hyperlipidemia"},"content":{"rendered":"\n

Introduction<\/strong><\/em><\/p>\n\n\n\n

 Syzygium campanulatum Korth (S. Campanulatum) <\/em>is an evergreen bush in the kingdom of Myrtaceae. In Malaysia and Singapore, it’s also known as “kelat paya,” and it’s commonly grown as a hedge. It is a typical decorative tree that is grown in public spaces like parks and roadways. When crushed, its leaves emit a cinnamon-like odor. Some of its regional names are pokok kelat paya, red lip, Chinese red-wood (Chinese name), Australian brush cherry, wild cinnamon, Ubah Laut (East Malaysia), and kelat oil. Despite its traditional use as a stomachic, no pharmacognostic or phytochemical profiling of S. campanulatum<\/em> has been reported to date, except for the isolation of betulinic acid. The fruits, which resemble blackberries, are visible from December to January and April to May. The shades of the juvenile leaves and flowers distinguish the two kinds of S. campanulatum:<\/em> one has yellow foliage and white-creamy flowers, while the other has red foliage and red blossoms. It contains different phytoconstituents such as flavonoids, phenolics, antioxidants, and betulinic acid. Leaves are known for hepatoprotective, antiangiogenesis, and anticancer properties.1,2<\/sup><\/p>\n\n\n\n

Hyperlipidemia is characterized as an elevation in the blood’s TG, TC, and LDL-C concentrations.3,4 <\/sup>It is a severe risk factor for cardiovascular illnesses, in particular atherosclerosis, coronary heart disease, and hypertension, according to various studies.5<\/sup> Hyperlipidemia is characterized by an abnormal elevation in the major circulatory lipids and lipoproteins; this adversely affects the pathways of cholesterol transport.6,7<\/sup> Increased formation of free radicals\/reactive oxygen species in hyperlipidemic conditions is known to participate in cardiac dysfunction, CVD progression, cardiac apoptosis, and necrosis.7,8<\/sup> Theconstancy of hyperlipidemia is influenced by a variety of causes, including ethnicity, genetic background, lifestyle factors such as poor dietary and exercise habits, poorly controlled diabetes, excessive alcohol consumption, and stress are all examples of risk factors. These diseases are caused by an increase in the consumption of a high-fat diet, which harms human health and life.9<\/sup><\/p>\n\n\n\n

Several classical hypolipidemic medicines are commonly used in clinical practice to treat this illness, including fibrates, nicotinic acid, its derivatives, bile acid sequestrants, and HMG-CoA reductase inhibitors. However, these medications can cause skeletal muscle toxicity, cutaneous flushing, decreased renal function, liver toxicity, and gastrointestinal discomfort in patients. As a result, new effective hypolipidemic medications with fewer (or no) side effects are urgently needed.10 <\/sup>Elevated blood triglyceride and cholesterol levels are the key risk factor for atherosclerosis, according to the American Heart Association. As a result, therapists consider hyperlipidemia therapy to be one of the most important strategies for slowing the atherogenic process.11,12<\/sup> Because of their low toxicity and health benefits, phytomedicines are becoming more popular, and they are suitable for long-term use as a dietary functional food. Flavonoids may help prevent and treatment of overweight, dyslipidemia, diabetes, and atherosclerosis, according to findings from preclinical pharmacologic tests and epidemiological investigations.13-16<\/sup> Phytomedicines might thus play a crucial part in the establishment of innovative treatment techniques. Therefore, the current study investigates the anti-hyperlipidemic action of the polyphenol-rich ethanolic leaf extract of S.Campanulatum<\/em> against triton and atherogenic diet-induced hyperlipidemia in experimental rats.<\/p>\n\n\n\n

Materials and methodology<\/strong><\/p>\n\n\n\n

Drugs, Reagents, and Chemicals<\/strong><\/p>\n\n\n\n

 Experimental hyperlipidemic\ndiet: Triton WR-1339 was obtained from Sigma-Aldrich, Experimental feed\ncontaining a well-powdered mixture of cholesterol (2%) was Procured from Loba\nChemie Pvt. Ltd., cholic acid (1%) and peanut oil (10%) from Sisco Research\nLaboratories Pvt. Ltd., sucrose (40%) from Merck Life Science Pvt. Ltd., and\nnormal laboratory diet (47%) (figure 3a). Atorvastatin was obtained from a\nlocal pharmacy. Total cholesterol, HDL, LDL, and Triglyceride kits were\nprocured from Agappe diagnostics Ltd (Kerala, India).<\/p>\n\n\n\n

Collection of Plant Materials<\/strong><\/p>\n\n\n\n

Syzygium campanulatum<\/em> fresh leaves werecollected from Udupi Manjunath\nMelkaje medicinal garden. The leaves were authenticated by DR H.S Shenoy,\nPrincipal scientist and Head of the division, Pilikula nisargadhama, Mangalore.\nVoucher specimen (9489\/Syzygium campanulatum Korth<\/em>.)   <\/strong><\/p>\n\n\n\n

Preparation of ethanol extract<\/strong><\/p>\n\n\n\n

After\ncollecting the leaves, they were placed in a clean tray and dried in the shade.\nBy utilizing a dry grinder, the dried leaves were reduced in size to a coarse\npowder and then sieved (20 Mesh). The powdered sample was extracted by using\nSoxhlet Apparatus with ethanol.<\/p>\n\n\n\n

Experimental animals<\/strong><\/p>\n\n\n\n

 The\nmale adult Wistar albino rats with body weights 170-220 g was used as\nexperimental animals. Rats were procured from CPCSEA-approved breeders and\nmaintained at CPCSEA approved institute animal house of Yenepoya University.<\/em> The study protocol was\napproved by the Institutional Animal Ethical Committee Yenepoya medical college\n(YU \/IAEC \/8\/2020) and the study was initiated only after the approval of the\ninstitutional animal ethics committee. The rats used in the experiment were\ncategorized into five groups, consisting of six rats each (60 Numbers).<\/p>\n\n\n\n

Tritron induce hyperlipidemia model (n=6)<\/strong><\/p>\n\n\n\n

Group 1:\nNormal control pre-treatment with vehicle<\/p>\n\n\n\n

Group 2: Disease control (Triton WR-1339 (400 mg\/kg))<\/p>\n\n\n\n

Group\n3: Standard drug  Atorvastatin\n10 mg\/kg<\/p>\n\n\n\n

Group\n4: Low dose of S. Campanulatum<\/em> 250\nmg\/kg<\/p>\n\n\n\n

Group\n5: High dose of S. Campanulatum<\/em> 500\nmg\/kg<\/p>\n\n\n\n

After fasting\n24hrs rats were treated with triton at a dose of 400 mg\/kg i.p, the\nhyperlipidemia was induced with triton WR-1339 for all groups except the normal\ncontrol group. The treatment of S. Campanulatum <\/em>250\/500 mg\/ml, <\/em>was\nadministered immediately following the triton injection, and the second dose of\nextracts was given 20 hours later.<\/p>\n\n\n\n

Atherogenic diet-induced hyperlipidemia model (n=6)<\/strong><\/p>\n\n\n\n

 Group 1: Normal control pre-treatment with\nvehicle<\/p>\n\n\n\n

Group 2: Disease control (atherogenic diet)<\/p>\n\n\n\n

Group\n3: Standard drug (Atorvastatin (dose of 10 mg\/kg<\/em>)) + atherogenic diet). 17<\/sup><\/p>\n\n\n\n

Group\n4: Low dose of S. Campanulatum<\/em> (250\nmg\/kg) + atherogenic diet<\/p>\n\n\n\n

Group\n5: High dose of S. Campanulatum<\/em> (500\nmg\/kg) + atherogenic diet<\/p>\n\n\n\n

For\nthe 20 days of the period, an atherogenic diet was mixed with a standard pellet\nand given to rats. The treatments were\nstarted on the 8th<\/sup> day of the atherogenic diet and continued till\nthe 20th<\/sup> day, a total of 14 days oftreatment of S. Campanulatum<\/em>\nextracts (250\/500 mg\/kg) was given. <\/p>\n\n\n\n

Blood collection and biochemical parameter analysis and estimation of liver enzymes <\/strong><\/p>\n\n\n\n

In\ntriton induced hyperlipidemia model 4 hours after the second dosage, blood\nsamples were drawn, and serum was separated from the blood for evaluation of\nlipoproteins. The hyperlipidemia was induced with an atherogenic diet model\n 48 h after the last dose blood samples were collected via cardiac\npuncture technique and centrifuged at 2500rpm for 10 minutes and the blood\nserum was collected and utilized to analyze biochemical parameters and\nestimation of liver enzymes and the standard diagnostic kits and semi\nautoanalyzer instrument was used for evaluation of lipoproteins (HDL,\ntriglycerides, LDL, total cholesterol), liver enzymes (SGOT, SGPT, ALP, and\nLDH) and tissue antioxidants (superoxide dismutase, catalase, thiobarbituric\nacid reactive species, and glutathione).18<\/sup><\/p>\n\n\n\n

In vivo antioxidant enzymes assay and histological Analysis<\/strong><\/p>\n\n\n\n

Immediately\nfollowing sacrifice, a tiny part of the liver tissues from each rat group was\nremoved and with ice-cold phosphate buffer it was homogenized for estimation of\ntissue antioxidants was performed using a UV spectrophotometer (SHIMADZU 1900),\nand other parts of the liver tissues of each group were fixed for\nhistopathology study in 10% formalin were prepared with pH of 7.4 phosphate\nbuffer kept at room temperature for 24 hours. Before being examined under a\nlight microscope, tissue-fixed slides were stained with hematoxylin and eosin.<\/p>\n\n\n\n

Statistical analysis<\/strong><\/p>\n\n\n\n

The data were\npresented as mean\u00b1SEM and were analyzed using one-way ANOVA followed by\nTukey-Kramer multiple comparison tests, with P<0.05 considered statistically\nsignificant. The statistical program used for data analysis was GraphPad\nPrism 6.01.<\/p>\n\n\n\n

Results and discussion<\/strong><\/p>\n\n\n\n

Ethanolic extraction and Phytochemical screening<\/strong><\/p>\n\n\n\n

In the current study, the percentage yield was obtained at 18% and AishaFA et al.,<\/em> (2013)performed a study on S.Campanulatum<\/em> methanolic extract was obtained with a percentage yield (16.4 percent, w\/w) compared to this study in the present study percentage yield was higher i.e. in the percentage yield is high in ethanolic extracts than methanolic extract. The qualitative phytochemical results showed the existence of alkaloids, flavonoids, steroids and triterpenoids, cardiac glycosides, carbohydrates, phenol, saponin, and tannins.<\/p>\n\n\n\n

Effect of extracts on serum lipid level<\/strong><\/p>\n\n\n\n

The increased\nblood lipid concentration is a significant modifiable dangerous factor for\ndeveloping atherosclerosis and cardiovascular disease. It is a class of\nmetabolic diseases characterized by a rise in blood lipid levels. Cholesterol,\ncholesterol esters, phospholipids, and triglycerides are examples of lipids.\nLDL cholesterol levels that are elevated are linked to the development of\natherosclerosis.<\/p>\n\n\n\n

Effect of extracts on triton-induced hyperlipidemia<\/strong><\/p>\n\n\n\n

The\nhyperlipidemia induced by triton is via several mechanisms, primarily by\ninhibiting lipoprotein lipase activity, preventing their uptake from\ncirculation through extrahepatic tissues, resulting in an increased level of\ncirculating lipoproteins, which can result in the blockage of TG-rich\nlipoprotein clearance. A single dose of triton in experimental animals increased\nserum lipid levels.19,20<\/sup> which was compared to our study the\nexperimental animals were injected with alone triton WR-1339 400 mg\/kg led to\nthe elevation of serum triglyceride 1021.455\u00b13.986, cholesterol 304.892\u00b13.825,\nLDL-C 32.931\u00b14.003 level, and decreased HDL-C 0.139\u00b10.031 values in rats when\ncompared with normal control rats triglyceride 48.749\u00b11.524, cholesterol\n41.181\u00b10.998, LDL-C 0.903\u00b10.209 and HDL-C 2.178\u00b10.264. At this time, in the\nrats treated with S.Campanulatum<\/em> 250 and S.Campanulatum<\/em> 500\nmg \/kg and standard drug atorvastatin10 mg\/kg significant serum lipid-lowering\neffect was observed triglyceride 738.359\u00b13.348, 80.505\u00b13.840 59.900\u00b10.649,\ncholesterol 171.823\u00b11.821, 48.141\u00b12.905, 49.758\u00b10.918, LDL-C 20.798\u00b12.570,\n6.697\u00b12.041, 10.758\u00b11.825 when compared to triton 400 mg\/kg and increased level\nof HDL-C 0.831\u00b10.050, 1.822\u00b10.154 and 1.136\u00b10.092 was also observed. S.Campanulatum<\/em> hypolipidemic activity\ncould, therefore, either increase the activity of lipolytic enzymes or\nstimulate fecal bile acid excretion, resulting in lower circulating lipoprotein\nlevels. 21,22<\/sup><\/p>\n\n\n\n

S. Campanulatum<\/em> appears to have no negative effects in normal rats based on its\neffects on organ function markers and other biochemical indices, and it is\npharmacologically effective and independent of negative side effects in\nhyperlipidemic rats with impaired cardiac, hepatic, and renal functions.\nincreased serum creatinine levels as a defense against kidney damage.23,24<\/sup>\nThe histopathological investigation of the liver segment of the normal control\nrats (Fig. 4a) revealed normal hepatic cell arrangements with no changes.\nHistopathological investigation of the liver section of rats treated with\ntriton 400 mg\/kg treated group (Fig. 4b) revealed that different degrees of\npathological changes such as the nucleus was absent, there is degeneration of\nfat in the center lobules, hepatic cell necrosis, and cloudy swelling. The\nmicroscopic examination revealed that in rats treated with S.Campanulatum<\/em>\n250 mg\/kg (Fig.4c), there is moderate damage in liver cells some nucleus are\nabsent but there was the recovery of the damaged cells to normal. The liver\nsection of rats treated with S.Campanulatum<\/em> 500 mg\/kg and atorvastatin\n10 mg\/kg (Fig. 4d, 4e,) revealed that\nnear normal arrangement hepatic cells and central vein were present, the\nresults are related to the normal control group.<\/p>\n\n\n\n

Effect of extracts on diet-induced hyperlipidemia<\/strong><\/p>\n\n\n\n

Induction of\nhyperlipidemia with atherogenic diet rats showed hair fall (Figure 3b) and the\npresence of extended adipose tissue in their intra-abdominal space and fatty\nliver were seen in the rats treated with atherogenic diet as compared to normal\ncontrol rats where abdominal space consist of normal fats and normal liver\norgan and the rats treated with extracts recover from the hair fall and\nintra-abdominal fat was reduced as compared to atherogenic diet groups (Figure\n3c). Jayant S et al.,<\/em> (2012)noticed\nthat providing all the animals with repeated administration of cholesterol\nand cholic acid (dissolved in ground nut oil) for 28 days elevated the main\nlipid profile parameters, including LDL-C, TG, VLDL-C, cholesterol, and\ndecreased HDL-C.17<\/sup> The atherogenic diet used in this\nstudy was also containing a mixture of cholesterol and cholic acid dissolved in\npeanut oil. The data shown in Table 1 represent that feeding rats with an\natherogenic diet caused a substantial (p < 0.001) rise in serum triglyceride\n335.036\u00b12.764, LDL-C 351.296\u00b12.187, total cholesterol 186.203\u00b11.328, and a\nsignificant (p < 0.001) reduction in serum HDL-C 0.245\u00b10.029 when compared\nto the control group. When compared to the atherogenic diet group, oral\nadministration of atorvastatin to rats resulted in a substantial (p < 0.001)\ndecrease in blood levels of triglyceride 154.120\u00b14.606, LDL-C 172.128\u00b11.649,\nand, total cholesterol 83.207\u00b13.818 as well as a significant (p < 0.001)\nrise in HDL-C 2.563\u00b10.032 levels. The hyperlipidaemic rats\nthat received S.Campanulatum<\/em> 250\/500 mg\/kg showed a significant (p\n< 0.001) decline in serum levels of triglyceride 254.940\u00b14.279,\n148.804\u00b12.655, total cholesterol 145.739\u00b11.352, 98.074\u00b12.681, LDL-C\n304.591\u00b12.661, 184.932\u00b14.768and substantial (p < 0.001) increase\nin HDL-C 1.556\u00b10.045, 2.4\u00b10.028 respectively, compared to rats on a high-fat\ndiet. Significant (p< 0.01) differences were identified between doses of\nboth plant extracts, indicating that this lipid-lowering action was\ndose-dependent.25<\/sup> However, the lipid-lowering impact of conventional\nmedicine (atorvastatin) was still greater than that of s.campanulatum<\/em> leaf extracts. A possible mechanism of\naction for S. campanulatum extracts is an increase in HDL-C, which is linked to\nthe mobilization of cholesterol from peripheral cells to the liver by the\nactivity of Lecithin Cholesterol O-acyltransferase (LCAT).26<\/sup> The\nLCAT enzyme is involved in the processes of HDL maturation, cholesterol flux\nfrom cell membranes into HDL, and cholesterol transesterification. Diet-induced\nhyperlipidemia tends to result in a decrease in enzyme activity. 27<\/sup><\/p>\n\n\n\n

Effects of extracts on liver function enzymes in an atherogenic diet-induced hyperlipidemic rat model<\/strong><\/p>\n\n\n\n

A chronic disease called nonalcoholic fatty liver disease has a strong correlation with obesity. Additionally, the emergence of a fatty liver is one of the most typical symptoms of those with hyperlipidemia. Various studies have shown that high-fat feeding caused laboratory animals to have decreased HDL-C levels and increased TC, TG, LDL-C, and Atherogenic index levels in their serum.28<\/sup> Thus, we also investigated S.Campanulatum’s<\/em> impact on liver lipids.The liver function enzymatic activities were evaluated in the control group, atherogenic diet group, and atherogenic diet rats were given the standard drug atorvastatin or extracts at two different doses for comparison (Table 1). When the disease group was compared to the normal control, there was a significant (p<0.001) increase in liver function enzymatic activities (SGOT, SGPT, ALP, LDH) in the atherogenic diet-induced hyperlipidemic rat group. The hyperlipidaemic rats receiving S.Campanulatum<\/em> 250\/500 mg\/kg revealed a substantial (p < 0.001) decline in serum levels of SGOT, SGPT, ALP, and LDH compared to rats of atherogenic diet control.29<\/sup> Furthermore, atorvastatin treatment improved the levels of SGOT, SGPT, ALP, and LDH in rats with atherogenic diet-induced hyperlipidemia.<\/p>\n\n\n\n

Table 1: Effect of S.Campanulatum<\/em> on SGOT, SGPT, ALP, and LDH in atherogenic diet-induced hyperlipidemia in Rats. <\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n
\n

  Treatment<\/strong><\/p>\n<\/td>\n

\n

    SGPT<\/strong><\/p>\n

    (IU\/L)<\/strong><\/p>\n<\/td>\n

\n

        SGOT<\/strong><\/p>\n

     (IU\/L)<\/strong><\/p>\n<\/td>\n

\n

    ALP<\/strong><\/p>\n

    (IU\/L)<\/strong><\/p>\n<\/td>\n

\n

         LDH<\/strong><\/p>\n

        (IU\/L)<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

N.Control<\/p>\n<\/td>\n

\n

64.547\u00b11.141<\/p>\n<\/td>\n

\n

114.385\u00b11.264<\/p>\n<\/td>\n

\n

166.513\u00b10.949<\/p>\n<\/td>\n

\n

293.246\u00b11.011<\/p>\n<\/td>\n<\/tr>\n

\n

Atherogenic diet<\/p>\n<\/td>\n

\n

131.946\u00b12.692***<\/sup><\/p>\n<\/td>\n

\n

229.769\u00b10.657***<\/sup><\/p>\n<\/td>\n

\n

690.201\u00b14.735***<\/sup><\/p>\n<\/td>\n

\n

769.417\u00b14.140***<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

S. Campanulatum<\/em>  250 mg\/kg<\/p>\n<\/td>\n

\n

113.970\u00b10.982abc<\/sup><\/p>\n<\/td>\n

\n

180.804\u00b10.855 abc<\/sup><\/p>\n<\/td>\n

\n

465.081\u00b14.761abc<\/sup><\/p>\n<\/td>\n

\n

513.496\u00b10.816abc<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

S. Campanulatum<\/em> 500 mg\/kg<\/p>\n<\/td>\n

\n

68.530\u00b12.014abc<\/sup><\/p>\n<\/td>\n

\n

144.776\u00b13.022 abc<\/sup><\/p>\n<\/td>\n

\n

249.081\u00b11.866abc<\/sup><\/p>\n<\/td>\n

\n

338.236\u00b10.776abc<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Atorvastatin 10 mg\/kg<\/p>\n<\/td>\n

\n

96.072\u00b10.791abc<\/sup><\/p>\n<\/td>\n

\n

120.802\u00b10.924 abc<\/sup><\/p>\n<\/td>\n

\n

179.966\u00b10.794abc<\/sup><\/p>\n<\/td>\n

\n

394.781\u00b10.813abc<\/sup><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

The results were reported as mean\u00b1SEM and analyzed using one-way ANOVA followed by Tukey-Karmer multiple comparison tests. Values were considered statistically significant when *<\/sup>P<0.05, **<\/sup>P<0.01, ***<\/sup>P<0.001 as compared to the normal group and a<\/sup>P<0.05, ab<\/sup>P<0.01, abc<\/sup>P<0.001 compared to the atherogenic diet group (n=6). SGPT- Serum Glutamic Pyruvic Transaminase, SGOT-Serum Glutamic Oxaloacetic Transaminase, ALP- Alkaline phosphatase, LDH- Lactate dehydrogenase.<\/p>\n\n\n

Effect of extracts on in vivo antioxidant enzymes in atherogenic diet hyperlipidemic rat model<\/strong><\/p>\n\n\n\n

It is known that high-fat diets cause more oxidative stress across different tissues, which may lead to some physically degenerative diseases. Although the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were assessed as indicators of serum or liver antioxidant capacities, the contents of malondialdehyde (MDA) in the serum or liver served as a marker to ascertain the lipid peroxidation levels in the serum and liver, respectively.28<\/sup> In this study Administration of an atherogenic diet for 5 weeks lowered the liver GSH level and at the same time increased the LPO. Treatment with extracts S.Campanulatum<\/em> 250\/500 mg\/kg replenished GSH levels and caused a decrease in LPO levels caused by the treatment of an atherogenic diet. The activities of the antioxidant enzyme SOD were decreased in atherogenic diet group administration compared to induced liver damage (Table 2). Treatment of the extracts counteracted the observed decrease in the activity of the enzyme.<\/p>\n\n\n\n

Table 2: Effect of S.Campanulatum<\/em> on in vivo<\/em> antioxidant enzymes in diet hyperlipidemic rat model.<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n
\n

Treatment<\/strong> <\/strong><\/p>\n<\/td>\n

\n

Glutathione<\/strong><\/p>\n

(\u00b5g\/mg protein)<\/strong><\/p>\n<\/td>\n

\n

LPO<\/strong><\/p>\n

(\u00b5g\/mg protein)<\/strong><\/p>\n<\/td>\n

\n

Catalase<\/strong><\/p>\n

(\u00b5g\/mg protein)<\/strong><\/p>\n<\/td>\n

\n

SOD<\/strong><\/p>\n

(\u00b5g\/mg protein)<\/strong><\/p>\n<\/td>\n<\/tr>\n

\n

N.Control<\/p>\n<\/td>\n

\n

77.213\u00b10.803<\/p>\n<\/td>\n

\n

6.535\u00b10.603<\/p>\n<\/td>\n

\n

95.390\u00b11.557<\/p>\n<\/td>\n

\n

24.873\u00b10.156<\/p>\n<\/td>\n<\/tr>\n

\n

Atherogenic diet<\/p>\n<\/td>\n

\n

2.121\u00b10.382***<\/sup><\/p>\n<\/td>\n

\n

26.101\u00b10.826***<\/sup><\/p>\n<\/td>\n

\n

21.053\u00b10.725***<\/sup><\/p>\n<\/td>\n

\n

4.308\u00b10.362***<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

S. Campanulatum<\/em>  250 mg\/kg<\/p>\n<\/td>\n

\n

22.926\u00b10.513abc<\/sup><\/p>\n<\/td>\n

\n

14.550\u00b10.377abc<\/sup><\/p>\n<\/td>\n

\n

49.691\u00b11.375abc<\/sup><\/p>\n<\/td>\n

\n

9.685\u00b10.763abc<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

S. Campanulatum<\/em> 500 mg\/kg<\/p>\n<\/td>\n

\n

57.308\u00b10.550abc<\/sup><\/p>\n<\/td>\n

\n

7.065\u00b10.374abc<\/sup><\/p>\n<\/td>\n

\n

78.726\u00b12.807abc<\/sup><\/p>\n<\/td>\n

\n

19.201\u00b10.710abc<\/sup><\/p>\n<\/td>\n<\/tr>\n

\n

Atorvastatin 10 mg\/kg<\/p>\n<\/td>\n

\n

65.668\u00b11.533abc<\/sup><\/p>\n<\/td>\n

\n

6.830\u00b10.626abc<\/sup><\/p>\n<\/td>\n

\n

89.180\u00b11.611abc<\/sup><\/p>\n<\/td>\n

\n

23.240\u00b10.291abc<\/sup><\/p>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

The results were reported as mean\u00b1SEM and analyzed using one-way ANOVA followed by Tukey-Karmer multiple comparison tests. Values were considered statistically significant when *<\/sup>P<0.05, **<\/sup>P<0.01, ***<\/sup>P<0.001 as compared to the normal group and a<\/sup>P<0.05, ab<\/sup>P<0.01, abc<\/sup>P<0.001 compare atherogenic diet group (n=6). LPO-Malondialdehyde, (Lipid peroxidation), SOD- Superoxide dismutase.<\/p>\n\n\n

Histopathological observation<\/strong><\/p>\n\n\n\n

Microscopical analysis of a liver segment from the normal control group (Fig. 5a) revealed normal hepatic cell organization. Microscopical examination of the atherogenic diet-treated group’s liver segment (Fig. 5b) revealed varying degrees of pathological alterations, including severe fatty degeneration, cloudy swelling, and hepatic cell necrosis, Boobalan Raja found comparable fatty changes in the hepatic tissue of hypercholesterolemic rats.30<\/sup> Histopathological study of rats treated with S.Campanulatum<\/em> 250 mg\/kg (Fig. 5c) showed less severe fatty changes compared to disease control. Some damaged hepatic cells were seen. Microscopical examination of S.Campanulatum<\/em> 500 mg\/kg treated group’s liver section (Fig. 5d) revealed mild fatty changes and recovery of damaged hepatic cells to normal. Rats given the standard drug (Fig. 5e) had normal hepatic cells and central veins, which were comparable to the normal control group.<\/p>\n\n\n\n\n\n
\"\"<\/td>\n\n

Figure 1: Effect of S.Campanulatum<\/em> on triton-induced hyperlipidemic rat\u2019s serum triglycerides, total cholesterol, LDL, and HDL level.<\/strong><\/p>\n

<\/p>\n

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Figure 2: Effect of S.Campanulatum<\/em> on atherogenic diet-induced hyperlipidemic rat’s serum total cholesterol, triglycerides, and phospholipids level.<\/strong><\/p>\n

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Figure 3: (3a) Atherogenic diet (3b) Hair loss during treatment and changes after treatment <\/strong>(3c) Difference between the pathology of liver of normal control, hyperlipidemic rats and rats treated with extracts.<\/strong><\/p>\n

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Figure 4: Effect of S.Campanulatum<\/em> on the morphology of liver in Triton 400 mg\/kg diet-induced hyperlipidemia in rats (magnification 40x).<\/strong><\/p>\n

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Figure 5: Effect of S.Campanulatum<\/em> on the morphology of liver in atherogenic diet-induced hyperlipidemia in rats (magnification 40x).  <\/strong><\/p>\n

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Conclusion<\/strong><\/p>\n\n\n\n

The present study concluded that this is the first study of the antihyperlipidemic activity of S.Campanulatum<\/em> ethanolic leaf extract. Ethanolic extract at a high dose (500 mg\/kg) has an effective reduction of hyperlipidemia in a triton and high atherogenic diet model, with comparable effects when compared to the Atorvastatin-treated group. The protective effect of plant extract is also revealed by histopathological studies. The active component in the plant may be able to reverse the lipid metabolic abnormalities seen in hyperlipidemia, however further research is needed to find out the active elements responsible for the activity and mechanisms of these benefits. As a result, it can be used as a therapeutic antihyperlipidemic drug or as an adjuvant to current hyperlipidemia treatment.<\/p>\n\n\n\n

Acknowledgment<\/strong><\/p>\n\n\n\n

The authors are thankful to the management of Yenepoya (Deemed to be University), Mangalore<\/p>\n\n\n\n

Conflict of Interest<\/strong><\/p>\n\n\n\n

There are no conflicts of interest regarding the publication of this article<\/p>\n\n\n\n

References:<\/strong><\/p>\n\n\n\n

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