Protective Effect of Ethanolic Extract of Seeds of Moringa oleifera Lam. Against Inflammation Associated with Development of Arthritis in Rats

Figures & data

TABLE 1 List of major phytochemical constituents of the seeds of Moringa oleifera

Active principles isolated/reported from seed extract	Reported activity	Reference
Alkaloid: Moringine	Relaxes bronchioles	Kirtikar and Basu (1975)
Flavonoids: Tocopherols, Vitamin C, polyphenols	Antioxidant	Laandrault et al. (2001)
Glycosides: Benzylisothiocyanate (a glycoside of mustard oil), and its derivatives: 4 (4′-acetyl-L-rhamnosyloxy)-benzoisothiocyanate,	Anti-inflammatory External counter-irritant properties	Das et al. (1958)
4 [α -L-rhamnosyloxy], phenylacetonitrile, 4-hydroxyl phenylacetonitrile, and 4-hydroxyphenylacetamide	Mutagens	Villasenor et al. (1989, 1990) Villasenor (1994)
4-[α -L-rhamnosyloxy]	Antibiotic	Dayrit et al. (1990)
4-[α -L-rhamnosyloxy]phenylacetonotrile β -Carotene], sterols and lecithin	Antimicrobial	Njoku and Adikwu (1997)
O-ethyl-4-(∝-L-rhamnosyloxy)benzylcarbamate together with seven known compounds: niazimicin, niazirin, β -sitostrol, glycerol-1-1-(9-octadeca-noate), 3-O-(6′-O-oleoyl-β -D-glucopyranosyl)-β -sitosterol, and β -sitosterol-3-O-β-D-glucopyranoside	Antitumor promoting activity	Guevara et al. (1999)
Nutrients: Thiamine, riboflavin, nicotinic acid, folic acid, pyridoxine, ascorbic acid and ∝ -tocopherol	As nutritives, antioxidants	Dahot and Memon (1985)
Fats: Monopalmitic acid, oleic acid, trioleic triglycerides in seeds and oil	Undefined properties	Memon and Khatri (1987)

FIG. 1 Effect of MOEE on body weight over the total treatment period. Value is highly significantly different from non-arthritic control (* p < 0.001). Value different from diseased controls (at differing levels of significance; ^@ p < 0.001, ^# p < 0.01, ^$ p < 0.05). Values shown are the mean ± SEM from nonarthritic, disease control, and treatment regimen rats (n = 6 rats/group).

FIG. 2 Effect of MOEE on paw edema volume of rats. Value different from diseased controls (at differing levels of significance; ^@ p < 0.001, ^# p < 0.01, ^$ p < 0.05). Values shown are the mean ± SEM from non-arthritic, disease control, and treatment regimen rats (n = 6 rats/group).

FIG. 3 Effect of MOEE on arthritic index on Day 21 of the treatment regimens. Value different from diseased controls (at differing levels of significance; ^@ p < 0.001, ^# p < 0.01, ^$ p < 0.05). Values shown are the mean ± SEM from disease control and treatment regimen rats (n = 6 rats/group).

FIG. 4 Effect of MOEE on ESR using blood obtained on Day 21 of the treatment regimens. Value is highly significantly different from non-arthritic control (*p < 0.001); value highly different from diseased control (^@ p < 0.001). Values shown are the mean ± SEM from nonarthritic, disease control, and treatment regimen rats (n = 6 rats/group).

FIG. 5 Effect of MOEE on RF levels in serum obtained on Day 21 of the treatment regimens. Value is highly significantly different from non-arthritic control (*p < 0.001). Value different from diseased controls (at differing levels of significance; ^@ p < 0.001, ^# p < 0.01, ^$ p < 0.05). Values shown are the mean ± SEM from nonarthritic, disease control, and treatment regimen rats (n = 6 rats/group).

TABLE 2 Effect of MOEE on levels of inflammatory mediators in serum obtained on Day 21 of the treatment regimens

Control (Distilled water)	13.6 ± 2.1	56.7 ± 7.1	46.5 ± 2.6
Disease control	33.1 ± 2.7^b	151.3 ± 5.9^c	75.1 ± 3.6^b
RA + Dexa (5 mg/kg)	17.2 ± 3.4^b	89.5 ± 15.9^a	51.6 ± 4.4^b
RA + MO1 (100 mg/kg)	28.2 ± 3.9	133.5 ± 16.6	72.3 ± 3.8
RA + MO2 (200 mg/kg)	20.0 ± 2.5^a	96.1 ± 14.1^a	57.1 ± 3.2^a

Values (all in pg/ml) are expressed as mean ± SEM (n = 6/regimen). Comparisons were made (1) between Group I (non-diseased control) and Group II (RA; diseased control) (^b p < 0.01; ^c p < 0.001), and (2) between Group II and Groups III (dexamethasone-treated), IV (MO1-treated), and V (MO2-treated) (^a p < 0.05; ^b p < 0.01).

TABLE 3 Effect of MOEE on oxidative stress in arthritic rats on Day 21 of the treatment regimens

	Antioxidant enzymes		Pro-oxidant
Treatment groups	SOD (U/mg protein)	CAT (μ mole H2O2 consumed/min/mg protein)	GSH (μ g/mg protein)	MDA (μ mole per mg protein)
Control (Distilled water)	2.89 ± 0.09	129.0 ± 5.8	6.15 ± 0.02	2.58 ± 0.06
Disease control	3.80 ± 0.07^c	158.5 ± 6.4^b	6.16 ± 0.03	1.48 ± 0.08^c
RA+Dexa (5 mg/kg)	3.18 ± 0.06^c	132.5 ± 5.1^a	6.21 ± 0.01	2.43 ± 0.05^c
RA+MO1 (100 mg/kg)	3.61 ± 0.09	151.5 ± 6.9	6.18 ± 0.01	2.25 ± 0.07^c
RA+MO2 (200 mg/kg)	3.35 ± 0.06^b	138.3 ± 5.5^b	6.16 ± 0.02	2.41 ± 0.06^c

Values are expressed as mean ± SEM (n = 6/regimen). Comparisons were made (1) between Group I (non-diseased control) and Group II (RA; diseased control) (^b p < 0.01; ^c p < 0.001), and (2) between Group II and Groups III (dexamethasone-treated), IV (MO1-treated), and V (MO2-treated) (^a p < 0.05; ^b p < 0.01; ^c p < 0.001).

FIG. 6 Histopathological effects from the various treatments. On Day 21 synovial joint sections of treated and untreated CFA arthritis animals stained with hematoxylin-eosin. A. Shows typical pathological changes in arthritic joint with bone destruction, cartilage erosion, severe angiogenesis and infiltration of lymphocytic cells. B. Normal synovial joint. C. Shows less angiogenesis and mild lymphocytic infiltration by dexamethasone treatment. D. MO1 shows less lymphocytic infiltration but does not protected joint against angiogenesis. E. MO2 shows significant protection against lymphocytic infiltration, bone destruction and cartilage erosion.

indicates angiogenesis, ↑ indicates lymphocytic infiltration, and

shows bone and cartilage destruction.

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