Nonalcoholic fatty liver disease (NAFLD) has become notorious globally. Increasingly emerging evidence shows that NAFLD is strongly associated with inflammation, with proinflammatory cytokines such as interleukin-2 (IL-2), interleukin-6 (IL-6), and tumour necrosis factor-α (TNF-α) playing a vital role in its progression. In this work, an attempt was made to verify the anti-inflammatory activity of Ruzu herbal bitters (RHB), an antiobesity medicinal concoction, on NAFLD induced by a high-fat diet (HFD) in albino Wistar rats. Twenty-five (25) rats were divided into five groups as follows: Group 1, the normal control, was maintained on standard rat chow and received normal saline (1 ml/kg body weight (BW)/day) for twelve weeks. The other groups were maintained on HFD for twelve weeks. Thereafter, groups 2–5 were treated with pioglitazone (4 mg/kg BW/day), RHB (0.6 ml/kg BW/day), normal saline (1 ml/kg BW/day), and fenofibrate (10 mg/kg BW/day), respectively. The animals were sacrificed after the experimental period. Biochemical indicators of oxidative stress and inflammation were assayed in the liver according to standard methods. The histological features of the liver were also compared to assess liver damage. RHB significantly (p<0.05) reduced body weight and liver index, inhibited oxidative stress, boosted antioxidant enzymes by increasing the activity and level of SOD and GSH, reduced proinflammatory markers (IL-2, IL-6, TNF-α), and reversed histological alterations induced by NAFLD in rat liver. In conclusion, the anti-inflammatory activity of RHB in the prevention of NAFLD in rats has been confirmed.

Context: One of the world’s most widespread and frequent liver diseases is the non-alcoholic fatty liver disease (NAFLD). Aims: To evaluate the preventives activities of Ruzu herbal bitters (RHB), which is an anti-obesity therapeutic concoction used widely in Nigeria on high–fat diet (HFD) induced NAFLD in albino Wistar rats. Methods: A total number of twenty-five rats were isolated and divided equally into five groups. Group 1, the normal control group was placed on normal rat diet and normal saline (1 mL/kg body weight daily) for twelve weeks. The remaining four groups 2-5 were placed on HFD for twelve weeks; adding to the following treatment schedules by oral gavage: group 2 received pioglitazone 4 mg/kg daily, group 3 received RHB 0.6 mL/kg daily, group 4 received normal saline 1 mL/kg daily and group 5 received fenofibrate 10 mg/kg daily (s.c). The animals were sacrificed and biochemical markers of liver function, lipid profile, glycemic index, and histopathological assessment of the liver of the rats were determined. Results: Rat treated with RHB and other treated groups significantly (p<0.05) reduced the liver index, fasting blood glucose, and activities and concentrations of liver function enzymes and molecules when compared to untreated NAFLD group. Scoring of hepatic steatosis also showed the ameliorative role of the treatment on NAFLD. Conclusions: This study reveals that RHB and other treatment options assessed could prevent HFD–induced NAFLD and could be explored as another therapeutic approach to fenofibrate and pioglitazone in NAFLD management.

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