THE EFFECT OF PAXHERBAL BITTERS ON OXIDATIVE STRESS, PLASMA LIPID PROFILE, AND FASTING BLOOD GLUCOSE

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ABSTRACT

High consumption of a diet rich in salt has been implicated in causing oxidative stress, which is well known to be involved in the pathogenesis of lifestyle-related diseases such as hypertension, dyslipidemia, and diabetes. Medicinal plants and herbal products are rich in bioactive substances that has been suggested to have possible prophylaxis against diseases. The aim of this study was to investigate the effects of Paxherbal bitters (PHB) on oxidative stress states, lipid profile, and blood glucose levels in albino Wistar rats fed high-salt diet (HSD) made up of modified growers mash whose salt content has been increased to a minimum of 8%. To achieve this, this study investigated the impact of Paxherbal bitters (PHB) on markers of oxidative stress: (malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD)); dyslipidemia, and fasting blood glucose (FBG) levels in rat fed high-salt diet (HSD). The study also determined and compared the therapeutic effect of PHB and standard antihypertensive drug (Lisinopril) on the histopathology caused by the HSD, on heart, liver, kidney and aorta. Thirty rats were used in this study. Group I (Normal Control) was fed normal diet, group II (negative control) was fed HSD; group III, (positive control) was fed HSD and administered Lisinopril (0.14 mg/kg) body weight; group IV, V, and VI were fed HSD and administered PHB (0.57ml/kg, 1.14ml/kg, and 1.71ml/kg) body weight respectively using an oro-gastric gavage for six weeks. Malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD), total cholesterol (TC), high density lipoprotein cholesterol (HDL-c), triglycerides (TG), low density lipoprotein cholesterol (LDL-c), very low density lipoprotein cholesterol (VLDL-c), FBG were all analysed using standard methods in the reagents kits as specified by the manufacturers. The result showed that PHB prevented a significant increase (P<0.05) in FBG of the rats in a dose dependent manner (55.80 ± 5.39, 53.20 ± 3.99, 50.60 ± 3.16) mg/dl from group IV, V, and VI respectively as compared to negative control (101.60 ± 7.77 mg/dl). The doses of PHB also caused a significant increase (P<0.05) in SOD and CAT when compared to the negative control. An increase in the level of MDA (17.56 ± 8.37, 10.46 ± 1.96, 10.82 ± 2.81) mmole/mg; and a decrease in the level of GSH (3.02 ± 0.13, 3.20 ± 0.27, 3.82 ± 0.12) U/mL in group IV, V, and VI respectively were significantly prevented (P<0.05) by PHB when compared to negative control (83.96 ± 9.56) mmole/mg; and (1.57 ± 0.05) U/mL for MDA and GSH respectively. Paxherbal bitters significantly decreased TC  (142.20 ± 5.82, 134.13 ± 2.13, 115.75 ± 3.77 mg/dl), TG (69.04 ± 3.39, 67.59 ± 2.05, 54.53 ± 4.44 mg/dl), VLDL-c (13.80 ± 0.68, 13.52 ± 0.41,10.86 ± 0.87mg/dl), and LDL-c (61.54 ± 6.40, 49.02 ± 2.43, 27.95 ± 3.65 mg/dl) when compared to negative control (229.05 ± 6.86 mg/dl, 124.01 ± 6.75 mg/dl, 24.80 ± 1.35 mg/dl, 162.89 ± 5.50 mg/dl) for TC, TG, VLDL-c, and LDL-c respectively. Histopathological examination of the tissues also corroborated the biochemical assays as observed in the non-disruption in the liver, kidney, and heart architecture as compared to the negative control. The Paxherbal bitters at all doses was effective in countering the deleterious effect of HSD by acting as an antioxidant, hypolipidaemic, and hypoglycaemic agent, which can be a prophylaxis against diseases caused by HSD induced hypertension.

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