Nephroprotective potential of Bacopa monniera on hypercholesterolemia induced nephropathy via the NO signaling pathway

Figures & data

Figure 1. Effect of AEBM on renal lipid status of HCD-induced hypercholesterolemia in control and experimental rats. Values were expressed as mean ± S.D. for six rats in each group. Statistical significance (p value): **p < 0.01, (a) compared with the control group, (b) compared with the HCD group.

Table 1. Effect of AEBM on the activities of renal enzymic antioxidant of HCD-induced hypercholesterolemia in control and experimental rats.

Groups	SOD	CAT	GPx	GR	GST
Control	3.11 ± 0.31	62.45 ± 6.77	14.34 ± 1.30	0.86 ± 0.07	0.56 ± 0.04
HCD	2.37 ± 0.28 a**	49.51 ± 5.14 a**	11.21 ± 1.10 a**	0.56 ± 0.06 a**	0.41 ± 0.02 a**
HCD + AEBM	2.90 ± 0.35 b**	56.78 ± 5.68 b**	13.14 ± 1.16 b**	0.72 ± 0.07 b**	0.49 ± 0.03 b**
AEBM	3.15 ± 0.30	61.56 ± 7.03	14.12 ± 1.34	0.83 ± 0.06	0.57 ± 0.07

Values were expressed as mean ± S.D. for six rats in each group. Statistical significance (p value): **p < 0.01, (a) compared with control group, (b) compared with HCD group.

SOD, units/mg protein, one unit is equal to amount of enzyme that inhibits the auto-oxidation reaction by 50%; CAT, µmoles of H₂O₂ consumed/min/mg protein; GPx, µg of GSH oxidized/min/mg protein; GR, µmol NADPH oxidized/min/mg protein; GST, nmol cDNB–GSH conjugate/min/mg protein.

Table 2. Effect of AEBM on the activities of renal non-enzymic antioxidant of HCD-induced hypercholesterolemia in control and experimental rats.

Groups	GSH	Vit-C	Vit-E
Control	8.34 ± 0.74	2.02 ± 0.19	1.62 ± 0.14
HCD	6.78 ± 0.59a**	1.44 ± 0.15a**	1.08 ± 0.12a**
HCD + AEBM	7.95 ± 0.64b**	1.81 ± 0.17b**	1.47 ± 0.15b**
AEBM	8.29 ± 0.86	2.10 ± 0.21	1.70 ± 0.17

Values were expressed as mean ± S.D. for six rats in each group. Statistical significance (p value): **p < 0.01, (a) compared with control group, (b) compared with HCD group. GSH, Vit C, Vit E: µg/mg protein.

Figure 2. Effect of AEBM on the levels in renal LPO of HCD-induced hypercholesterolemia in control and experimental rats. Values were expressed as mean ± S.D. for six rats in each group. Statistical significance (p value): *p < 0.05, **p < 0.01, (a) compared with the control group, (b) compared with the HCD group.

Table 3. Effect of AEBM on the levels of urea, creatinine, and uric acid (renal markers) in serum of HCD-induced hypercholesterolemia in control and experimental rats.

Groups	Urea (mg/dl)	Creatinine (mg/dl)	Uric acid (mg/dl)
Control	27.69 ± 2.47	1.08 ± 0.10	1.85 ± 0.19
HCD	40.34 ± 4.06a**	1.31 ± 0.15a**	2.95 ± 0.31a**
HCD + AEBM	32.04 ± 3.23b**	1.17 ± 0.13b**	2.15 ± 0.23b**
AEBM	28.15 ± 2.40	1.10 ± 0.11	1.94 ± 0.17

Values were expressed as mean ± S.D. for six rats in each group. Statistical significance (p value): **p < 0.01, (a) compared with the control group, (b) compared with the HCD group.

Figure 3. Effect of AEBM on mRNA expression levels of eNOS in renal artery of control and experimental rats. Lane 1 represents the DNA marker; lane 2 represents the control group; lane 3 represents the HCD group; lane 4 represents the HCD + AEBM treatment group; lane 5 represents the AEBM alone group. Densitometric analysis of the bands is expressed as net intensity ratio corrected for the corresponding β-actin contents. Values were expressed as mean ± S.D. for six rats in each group. Statistical significance (p value): *p < 0.05, **p < 0.01, (a) compared with the control group, (b) compared with the HCD group.

Figure 4. Effect of AEBM on mRNA expression levels of iNOS in renal artery of control and experimental rats. Lane 1 represents the DNA marker; lane 2 represents the control group; lane 3 represents the HCD group; lane 4 represents the HCD + AEBM treatment group; lane 5 represents the AEBM alone group. Densitometric analysis of the bands is expressed as net intensity ratio corrected for the corresponding β-actin contents. Values were expressed as mean ± S.D. for six rats in each group. Statistical significance (p value): **p < 0.01, (a) compared with the control group, (b) compared with the HCD group.

Figure 5. Effect of AEBM on histopathological changes in renal tissue of HCD-induced hypercholesterolemia in control and experimental rats. Transection of renal tissue (control) showed normal architecture of glomeruli and tubules of nephron (H&E, 100×) (Figure 5A). Transection of HCD-induced rats depict swelling of renal tubules and tubular epithelial denudation with casts in the widened lumens (glomerular hypertrophy) of renal tissue (Figure 5B). Transection of AEBM + HCD rats showed mild tubular epithelial damage when compared with HCD rats (Figure 5C), when compared with HCD rats. AEBM alone (Figure 5D)-treated rats showed normal renal architecture similar to that of control rats (H&E, 100×) (scale bar: 50 µm).