Results
Table 1 showed that oral administration of Diclofenac sodium at 150mg/kg.b.w. resulted in a significant increase in renal tumor necroses factor -α (TNF-α), nitric oxide (NO) and thiobarbaturic acid reactive substances (TBARS) compared to the normal control group (p< 0.01). Rat receiving extract of any of the two doses of cranberry extract used in this study (75 and 150mg/kg.b.w.) showed a significant decrease in renal TNF-α, NO and TBARS compared to the group that received Diclofenac sodium (p< 0.01). Also, supplementation of vitamin C at (1g/k.g.b.w.) resulted in a significant decrease in renal TNF-α, NO and TBARS compared to the group that received Diclofenac sodium (p< 0.01). Tables 2 and 3 showed that oral administration …show more content…
It was given to all groups except the normal one. Cranberry extract and vitamin C were orally given daily for 3 weeks and the last dose of each was given 1 h before Diclofenac sodium administration. Blood samples were collected 24 h after Diclofenac sodium administration. Values are given as mean ± SD for groups of eight animals each. * Significantly different from normal group at p< 0.01
Table 2: Level of blood reduced glutathione (GSH) and activities of superoxide dismutase (SOD) and catalase (CAT) in normal and experimental groups of rats.
No. Groups GSH
(mg %) SOD
(U/gm Hb) CAT
(U/gm Hb)
(I) Normal
1 % tween 80 23.64 ± 2.83 385.54 ± 18.65 95.22± 5.84
(II) Positive control
Diclofenac sodium (150 mg/kg.b.w) 8.90 ± 1.77* 167.25 ±9.24* 48.16 ± 4.41*
(III) Cranberry extract
(75 mg/kg.b.w.) 15.46 ± 2.17* 304.42 ± 11.68* 73.55 ± 4.08*
(IV) Cranberry extract (150mg/kg b.w.) 21.55 ± 3.06* 389.75 ± 21.38* 92.20 ± 4.59*
(V) Vitamin C (1g/kg,b.w) 19.80 ± 2.68* 360.32 ± 19.33* 80.05 ±
Table 1 showed that oral administration of Diclofenac sodium at 150mg/kg.b.w. resulted in a significant increase in renal tumor necroses factor -α (TNF-α), nitric oxide (NO) and thiobarbaturic acid reactive substances (TBARS) compared to the normal control group (p< 0.01). Rat receiving extract of any of the two doses of cranberry extract used in this study (75 and 150mg/kg.b.w.) showed a significant decrease in renal TNF-α, NO and TBARS compared to the group that received Diclofenac sodium (p< 0.01). Also, supplementation of vitamin C at (1g/k.g.b.w.) resulted in a significant decrease in renal TNF-α, NO and TBARS compared to the group that received Diclofenac sodium (p< 0.01). Tables 2 and 3 showed that oral administration …show more content…
It was given to all groups except the normal one. Cranberry extract and vitamin C were orally given daily for 3 weeks and the last dose of each was given 1 h before Diclofenac sodium administration. Blood samples were collected 24 h after Diclofenac sodium administration. Values are given as mean ± SD for groups of eight animals each. * Significantly different from normal group at p< 0.01
Table 2: Level of blood reduced glutathione (GSH) and activities of superoxide dismutase (SOD) and catalase (CAT) in normal and experimental groups of rats.
No. Groups GSH
(mg %) SOD
(U/gm Hb) CAT
(U/gm Hb)
(I) Normal
1 % tween 80 23.64 ± 2.83 385.54 ± 18.65 95.22± 5.84
(II) Positive control
Diclofenac sodium (150 mg/kg.b.w) 8.90 ± 1.77* 167.25 ±9.24* 48.16 ± 4.41*
(III) Cranberry extract
(75 mg/kg.b.w.) 15.46 ± 2.17* 304.42 ± 11.68* 73.55 ± 4.08*
(IV) Cranberry extract (150mg/kg b.w.) 21.55 ± 3.06* 389.75 ± 21.38* 92.20 ± 4.59*
(V) Vitamin C (1g/kg,b.w) 19.80 ± 2.68* 360.32 ± 19.33* 80.05 ±