Aim of the present study was to assess the hepatoprotective activity of goat milk on antitubercular drug-induced hepatotoxicity in rats. Hepatotoxicity was induced in rats using a combination of isoniazid, rifampicin, and pyrazinamide given orally as a suspension for 30 days. Treatment groups received goat milk along with antitubercular drugs. Liver damage was assessed using biochemical and histological parameters. Administration of goat milk (20 mL/kg) along with antitubercular drugs (Group III) reversed the levels of serum alanine aminotransferase (82 ± 25.1 vs. 128.8 ± 8.9 units/L) and aspartate aminotransferase (174.7 ± 31.5 vs. 296.4 ± 56.4 units/L, p<0.01) compared with antitubercular drug treatment Group II. There was a significant decrease in serum alanine aminotransferase (41.8 ± 4.1 vs. 128.8 ± 8.9 units/L, p<0.01) and aspartate aminotransferase (128.8 ± 8.54 vs. 296.4 ± 56.4 units/L, p<0.001) levels in Group IV (goat milk 40 mL/kg) compared with antitubercular drug treatment Group II. Goat milk (20 mL/kg and 40 mL/kg) was effective in reversing the rise in malondialdehyde level compared with the antitubercular drug suspension groups (58.5 ± 2 vs. 89.88 ± 2.42 μmol/mL of tissue homogenate, p<0.001 and 69.7 ± 0.78 vs. 89.88 ± 2.42 μmol/mL of tissue homogenate, p<0.001, respectively). Similarly, both doses of milk significantly prevented a fall in superoxide dismutase level (6.23 ± 0.29 vs. 3.1 ± 0.288 units/mL, p<0.001 and 7.8 ± 0.392 vs. 3.1 ± 0.288 units/mL, p<0.001) compared with the group receiving antitubercular drugs alone. Histological examination indicated that goat milk reduced inflammation and necrotic changes in hepatocytes in the treatment groups. The results indicated that goat milk prevented the antitubercular drug-induced hepatotoxicity and is an effective hepatoprotective agent.
Objective: Inflammatory bowel disease (IBD) is a disorder characterized by chronic inflammation of the gastrointestinal tract and its exact etiopathology is still unclear. Most of the currently available drugs provide the symptomatic improvement, and their long-term use can lead to various unwanted effects also. This study was done to observe the effects of vinpocetine alone and in combination with sulfasalazine on IBD in rats.Methods: Adult Wistar rats of either sex were used (n=36). Experimental colitis was produced by intracolonic administration of acetic acid (10% v/v, 0.20 ml/rat) given per rectally. Rats were divided into six groups (n=6): Group I - normal control (0.9% w/v saline, intracolonic administration + 0.5% w/v carboxymethyl cellulose, i.e., CMC, p.o); Group II - acetic acid (10% v/v, intracolonic administration+0.5% w/v CMC, p.o); Group IIIA - acetic acid + vinpocetine (5 mg/kg, p.o); Group IIIB - acetic acid + vinpocetine (10 mg/kg, p.o); Group IV - acetic acid + sulfasalazine (360 mg/kg, p.o.); Group V - acetic acid + sulfasalazine + vinpocetine (360 mg/kg, p.o. + 5 mg/kg, p.o). The study period was of 15 days in which animals were treated with acetic acid solution on day 1 and treatment was started 4 hrs after the administration of acetic acid till the 14th day. On 15th day, the animals were sacrificed for the investigation of various macroscopic, microscopic, and biochemical parameters.Results: The higher dose of orally administered vinpocetine (10 mg/kg) and combination of sulfasalazine + vinpocetine (360 mg/kg + 5 mg/kg) were found to be the most effective in reducing the severity of mucosal damage which was similar to the reference drug sulfasalazine (360 mg/kg). Both the doses of vinpocetine curtailed the histopathological scores. The combination therapy of sulfasalazine + vinpocetine (360 mg/kg + 5 mg/kg) was equally effective to standard drug but not found to be the most effective treatment. Myeloperoxidase levels were significantly reduced in vinpocetine treated groups as compared to acetic acid control group, while the glutathione levels were increased significantly. Similarly, vinpocetine significantly decreased the malondialdehyde level in the intestinal tissue of the rats with acetic acid induced colitis, and thus the severity of the tissue damage.Conclusion: The results of this study indicated that vinpocetine possesses anti-inflammatory activity and are therapeutically effective in acetic acid induced ulcerative colitis at a dose of 5 mg/kg. More pronounced effects were observed at higher dose, i.e., 10 mg/kg. The combination of sulfasalzine + vinpocetine was also found to be effective as compared to high dose of vinpocetine (10 mg/kg).
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