World Journal of Pharmacology and Toxicology
Open Access

Lipoprotein (a), is a particle in your blood which carries cholesterol, fats and proteins. The amount your body makes is inherited from one or both parents and is determined by the genes passed on from your parent(s) when you are born. It does not change very much during your lifetime except if you are women, levels increase as the natural estrogen level declines with menopause. Diet and exercise seems to have little to no impact on the lipoprotein (a) level.

Due to low compliance and adverse effects of conventionally used hypolipidemic agents, herbal medicines are going to be famous among Physicians, and Cardiologists. Medicinal herbs like Curcuma Longa, Fenugreek, and Lemon contents are being used as mild to moderate hypolipidemic agents. Curcuma Longa commonly known as Haldi in India and Pakistan is used to lower plasma lipids, in view of their contents. It contains Curcuminoids (curcumin, demethoxycurcumin, and bisdemethoxycurcumin), turmerone, atlantone, zingiberene, proteins, and resins. Coronary artery disease (CAD) occurs when the inside (the lumen) of one or more coronary arteries narrows, limiting the flow of oxygen-rich blood to surrounding heart muscle tissue. Atherosclerosis is the process that causes the artery wall to get thick and stiff. It can lead to complete blockage of the artery, which can cause a heart attack [1]. The disease process begins when LDL deposits cholesterol in the artery wall. The body has an immune response to protect itself and sends white blood cells called macrophages to engulf the invading cholesterol in the artery wall. When the macrophages are full of cholesterol, they are called foam cells because of their appearance. As more foam cells collect in the artery wall, a fatty streak develops between the intima and the media. If the process is not stopped, the fatty streak becomes a plaque, which pushes the intima into the lumen, narrowing the blood flow [2-6]. With few exceptions, low HDL is an independent risk factor for CAD in case-control and prospective observational studies [7]. In contrast, high HDL levels are associated with longevity and are protective against the development of atherosclerotic disease [8]. In the Framingham Study, risk for CAD increases sharply as HDL levels fall progressively below 40 mg/dL [9- 10]. In the Quebec Cardiovascular Study, for every 10% reduction in HDL, risk for CAD increased 13%. [2] Many clinicians believe that low HDL is associated with increased CAD risk because it is a marker for hypertriglyceridemia and elevated remnant particle concentrations. The Prospective Cardiovascular Münster Study, however, demonstrated that the increased risk associated with low HDL is independent of serum triglyceride levels [11]. There is considerable controversy about whether one HDL subfraction is more antiatherogenic than others. At the present time, the preponderance of evidence favors increasing total HDL mass, rather than any one subfraction of this lipoprotein [12].

Material and Method

The study was conducted at Ghurki trust teaching hospital, Lahore Pakistan from January 2018 to August 2018. 90 patients were selected for study. Consent was taken from all participants. An inclusion criterion was primary and secondary hyperlipidemic patients. An exclusion criterion was patients suffering from any kidney, liver and thyroid related disease. Name, age, gender, occupation, residential address, phone/contact number, previous medical history, disease in family history, drug history were recorded in specific Performa. Three groups I, II, and III were made (30 patients in each group). Group-I was allocated for placebo, to take placebo capsule once daily, after breakfast for six weeks. Group-II was advised to take 2 tea spoons of kalonji after breakfast for the period of six weeks. Group-III was on Niacin 2 grams in divided doses, after breakfast, lunch and dinner for 6 weeks. Their base line LDL-cholesterol and HDL-cholesterol level was estimated at the start of research work. Their serum was taken at follow up visits, fortnightly for lipid profile. Data were expressed as the mean ± SD and ‘t’ test was applied to determine statistical difference in results. A p-value > 0.05 was considered as non-significance and P-value < 0.001 was considered as highly significant change in the differences. Serum LDL-cholesterol was calculated by formula (LDLCholesterol= Total Cholesterol-(Triglycerides/5 +HDL-Cholesterol). Serum HDL-cholesterol was determined by using kit Cat. # 3022899 by Eli Tech Diagnostic, France.

Data Inference and Results

Numerical values and results of all parameters of participated patients were analyzed biostatistically. In placebo group, LDLcholesterol decreased from 189.15 ± 3.90 mg/dl to 186.75 ± 2.08 mg/dl, change in the parameter is 2.40 mg/dl. This difference in pretreatment and post treatment value is non-significant, i.e., P-value > 0.05. HDL-cholesterol in placebo group increased from 36.11 ± 2.11 mg/ dl to 37.17 ± 1.51 mg/dl. The difference in parameter was 1.06mg/dl. Statistically this change in parameter was non-significant i.e., P-value > 0.05. In Nigella sativa group, out of 30 hyperlipidemic patients, 27 patients completed over all study period. LDL-cholesterol in this group decreased from 202.45 ± 1.54 mg/dl to 189.52 ± 2.21 mg/dl. The difference in pretreatment and post-treatment mean values is 12.93 mg/ dl. Statistically this change in two mean values is highly significant, with p-value <0.001. HDL- cholesterol in this group increased from 38.81 ± 3.90 42.19 ± 3.32 mg/dl. Change in two mean values was 3.38 mg/dl. Statistically this change is significant, with probability value <0.01. In group III, 28 patients completed the research. LDL-cholesterol in this group decreased from 212.65 ± 2.32 to 185.61 ± 3.43 mg/dl in 6 weeks treatment. Change in pre and post treatment mean values is 27.04 mg/ dl. Statistically this change is highly significant, i.e., P-value < 0.001. HDL-cholesterol increased from 39.19 ± 2.01 to 43.00 ± 3.07 mg/dl in 6 weeks. Change in two parallel values is 3.49 mg/dl, which is significant with P-value <0.01 (Table 1).

Key: HDL and LDL are measured in mg/dl, n stands for sample size, p-value >0.05 indicate non-significant, <0.01 indicate significant and <0.001 indicate highly significant change in basic values

Table 1: LDL, HDL’s basic values (pre and after treatment) and their biostatistical significance

Cholesterol is produced naturally in your liver because every cell in your body uses it. Similar to triglycerides, cholesterol is also found in fatty foods like eggs, red meat, and cheese. Hyperlipidemia is more commonly known as high cholesterol. Although high cholesterol can be inherited, it’s more often the result of unhealthy lifestyle choices. Treatment with three weeks, Kalonji decreased LDL-cholesterol 12.93 mg/dl by six weeks of treatment. HDL-cholesterol increased 3.38 mg/ dl by taking this drug for six weeks. The changes in both parameters were significant.

In placebo group, LDL-C reduction was 2.40 mg/dl and increase in HDL-C was 1.06 mg/dl with P-value >0.05, which proves nonsignificant change in results. These results match with Akhondian et al. [13] who did prove that Nigella sativa is very effective hypolipidemic drug. He tested the drug on 120 hyperlipidemic and diabetic patients by using Nigella sativa for one month. Their results were highly significant when compared with placebo-controlled group. Our results also match with results of Gillani AH et al. [14] who proved LDLCholesterol reduction from 201.61 ± 3.11 mg/dl to 187.16 ± 2.10 mg/ dl in 40 hyperlipidemic patients. Their HDL-C increase was 3.98 mg/dl which also matches with our results. Results of our study are in contrast with results of research work conducted by AH BH and Blunden G [15]. They explained that some active ingredients of Nigella sativa are hypolipidemic but their hypolipidemic effects are very narrow spectrum. Their results showed only 2.11 mg/dl change in LDL-C and 0.92 mg/dl increase in HDL-C of 38 rats. Difference in results may be genetic variants of human and rats. Brown BG et al. [16] also described phenomenon of genetic variation in pharmacological effects of Nigella sativa. Burits M and Bucar F [17] have also mentioned wide variety effects of Nigella sativa with different genetic make ups. Our results also match with results of research work of Dehkordi FR, Kamkhah AF [18] and El-Dakhakhany M [19]. Same mechanism of action of drug Nigella sativa is described by El-Din K et al. [20]. In our research reduced LDL-Cholesterol from 212.65 ± 1.19 mg/dl to 185.61 ± 1.65 mg/dl in six weeks. This reduction in LDL-C was 27.04 mg/dl, which is highly significant change, when analyzed statistically. These results match with results n of research work conducted by Afilalo J et al. [21] who proved almost same change in LDL-C in 32 hyperlipidemic patients who were cases of secondary hyperlipidemia and used Niacin 2 grams daily for 2 months. Their LDL-C reduction was 25.55 mg/ dl. Their HDL-C increase was 6.65 mg/dl in 2 months. In our results HDL-C increase was 3.81 mg/dl in six weeks use of Niacin. Our results also match with results of research conducted by Whitney EJ et al. [22] who proved 27.77 mg/dl reduction in LDL-C in 19 hyperlipidemic patients. Ginsberg HN et al. [23] also support our results, as they proved 4.00 mg/dl increase in HDL-C when 2 grams of Niacin was used in 34 hyperlipidemic patients for 6 weeks. Our results do not match with results of research conducted by Boden WE et al. [24] who proved that 2.5 grams Niacin decreased 10.99 mg/dl LDL-Cholesterol. HDL-C increase was only 1.11 mg/dl. These differences may be considered due to lack of physical exercise and no restriction of use of lipids in their diet. Taylor AJ et al. [25] used Niacin 1.5 grams in 29 hyperlipidemic patients for 3weeks. Patients reduced their LDL-C from 189.88 ± 1.11 mg/dl to 187.87 ± 0.99 mg/dl. Difference in their results and our results is due to less sample size, lesser duration of exposure of patients to drug and small amount of drug given in their patients. Baigent C et al. [26] explained that Niacin inhibits the peripheral mobilization of free fatty acids, which decreases the substrate available for hepatic synthesis of triglycerides and very low-density lipoprotein (VLDL) particles.

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