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Effect of lime juice extract of cashew bark on lipid biomarkers in indomethacin-induced gastric ulcerated Wistar rats
Abstract
This study investigated the effect of lime juice extract of cashew bark (LJECB) on lipid profile in indomethacin-induced gastric ulcer in Wistar rats. Freshly pulverised Anacardium occidentale stem bark (1 kg) was soaked in freshly prepared Citrus aurantifolia fruit juice (3 L) for 48 hours inside a refrigerator (4 oC). The filtered solution was concentrated in vacuo using rotary evaporator to produce the crude extract labeled as LJECB. Forty-two (42) female Wistar rats (100-150 g) were randomized into seven groups (n = 6) and treated as follow. Group 1: normal control (Distilled water 1 ml/100g body weight); Group 2: 30 mg/kg indomethacin Only (ulcerated group); Group 3: 30 mg/kg indomethacin + 0.2 ml/kg Antacid; Group 4: 30 mg/kg indomethacin + 400 mg/kg LJECB; Group 5: 30 mg/kg indomethacin + 800 mg/kg LJECB. Group 6: 400 mg/kg LJECB; Group 7: 800 mg/kg LJECB. Prior to ulcer induction, the animals were fasted overnight and allowed free access to water ad libitum. Then indomethacin (30 mg/kg, 1 ml) was orally administered to the rats in Group 2 - 5. Treatment with LJECB or antacid commenced 4 hours post-induction for 14 days. After the last dose, the animals were fasted overnight and sacrificed under mild inhalation of diethyl ether. Serum samples were prepared and used for lipid biomarker analyses (total cholesterol, triglycerides, HDL-c, LDL-c, and VLDL-c). Castelli risk index-1 and 2 were calculated from an established equation to determine the cardiovascular risk of the extract. Results showed that the untreated ulcerated group had a significant reduction in total cholesterol levels compared to the normal control group. Treatment with a high dose of LJECB further caused a significant decrease in the total cholesterol levels. Also ulcerated group had a significant reduction in triglyceride levels compared to the normal control group. Treatment with 400 mg/kg dose of LJECB further lowered the triglyceride levels in ulcerated rats, however, higher dose of LJECB (800 mg/kg) increased the triglyceride levels. Untreated ulcerated rats had a significant increase in HDL compared to the normal control group. Administration of LJECB (400 mg/kg) had no significant (p<0.0001) effect on HDL levels in the ulcerated group. However, 800 mg/kg of LJECB administered to a normal control group was associated with an increase in HDL. Moreover, the LDL was significantly low across all the groups. The normal control group had a higher Castelli risk index-1 (CRI-1), while the ulcer group and LJECB-treated groups had a relatively lower CRI-1 value. The study concludes that administration of LJECB to Wistar rats was associated with a reduction in total cholesterol and LDL levels, elevated HDL levels, and low Castelli risk index, in both ulcerated and non-ulcerated rats.