Roasted cashew nut supplement inhibits MCP-1 and inflammatory mediators to correct hypertension related liver failure induced by mixed-fractionated petroleum products via NOS-cAMP-PKA signaling pathway in male rats

Abstract

People who expose to mixture of crude oil products had been reported to show several diseased-symptoms including hypertension, liver failure and chronic complications. The drugs for treating multiple-complex diseases are scarcely available. Cashew nut snack is known to check multiple diseases and easily accessible by indigenous-patients with no lethal-effects. Here, we examined the corrective-measures of roasted-cashew-nut (RCN) against hypertension co-morbidity with liver-failure in male rats on exposure to mixture of fractionated-petroleum-products (MFPP). Seventy (70) male-albino-rats (n=10) were randomly exposed to MFPP for 14 days. Group 1: control rats were given basal-diet. Group 2 was given basal diet + 0.2ml/day-MFPP. Group 3 was given 0.2ml/day-MFPP + 50 mg/kg Atenolol. Group 4 was given 0.2ml/day-MFPP + 10% RCN. Group 5 was given 0.2ml/day-MFPP + 20% RCN. Group 6 was given 10% RCN. Group 7 was given 20% RCN. We found that high activities of liver-arginase, MAO-A, AChE, ADA, PDE-51 and ATP-hydrolytic-enzymes with low-bioavailability of NO-level on exposure to MFPP implicated liver-failure and hypertension. Also, up-regulation of HIF-1, p53, TNF-α, and MCP-1 with reduced-level of 1L-10 were connected to liver-failure and hypertension. However, post-treatment with 10% RCN and 20% RCN for 14-days corrected liver-failure and hypertension by inhibiting liver-arginase, MAO-A, AChE, ADA, PDE-51 and ATP-hydrolytic-enzymes. Also, liver-failure characterized by vascular-congestion and sinusoidal-dilation on exposure to 0.2ml/day-MFPP was reversed by 10% RCN and 20% RCN via down-regulation of liver HIF-1, p53, TNF-α, MCP-1 with increased 1L-10. We conclude that 10% RCN and 20% RCN may be an innovative-snacks against hepatocellular damage co-morbidity with hypertension.