Anti-inflammatory and analgesic activities of methanol extract of Helianthus annuus Linn. (Asteraceae) leaf
Article Category: Research Article
Pubblicato online: 24 apr 2019
Pagine: 112 - 116
DOI: https://doi.org/10.2478/ebtj-2019-0013
Parole chiave
© 2019 Samuel O. Onoja, Glory C. Onyebuchi, Ifeoma I. Ijeh, Maxwell I. Ezeja, published by Sciendo
This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.
Inflammation is an immunological reaction and implicated in the pathophysiology of many disease conditions (1, 2). Uncontrolled inflammatory reaction may aggravate pathological conditions and it is marked with pain, swelling, heat, redness and loss of function (3). Inflammatory processes are suppressed with anti-inflammatory drug in medical practice. Ethnomedical preparations improves clinical disease conditions by suppression of inflammatory processes (4-6).
The leaf of
One hundred and twenty (120) Wistar albino rats of both sexes weighing 100-115 grams were used for this experiment. The environmental condition of the animal house and other management practices were as explained by Onoja
The presence of tannins, saponins, alkaloids, flavonoids, glycosides and terpenes were determined using standard methods of Trease and Evans (16).
The
The antinociceptive properties of HAE was evaluated as described by Onoja
The results were presented as mean ± standard error of mean (SEM). Data obtained were analyzed using one way analysis of variance (ANOVAs) and the variant means were separated by Least Significant Difference (LSD) of the different groups. Significance was accepted at the level of p < 0.05.
The percentage yield of the HAE was 10.31%.
The test revealed the presence of tannins, saponins, alkaloids, flavonoids, glycosides and terpenes.
The HAE elicited significant (P < 0.05) decrease in the paw volume in the treated groups when compared with the negative control group. At 3 h post treatment, the reduction in paw volume of ASA, HAE 150, 300 and 600 mg/kg treated groups were 36.36%, 24.24%, 33.33% and 33.33% reduction in paw volume, respectively when related to the negative control. The percentage inhibition in paw volume of HAE (300 and 600 mg/kg) treated groups were not significant (p > 0.05) compared to ASA treated group (
Formalin-induced paw edema
| Treatment (n = 6) | Mean increase in paw volume in ml ± SEM (% inhibition) | ||
|---|---|---|---|
| 1 h | 2 h | 3 h | |
| 5% Tween-20, 10 ml/kg | 0.39 ± 0.02 (-) | 0.44 ± 0.04 (-) | 0.33 ± 0.04 (-) |
| ASA 200 mg/kg | 0.27 ± 0.02*(30.77) | 0.21 ± 0.02*(52.27) | 0.21 ± 0.01*(36.36) |
| HAE 150 mg/kg | 0.36 ± 0.03 (7.69) | 0.29 ± 0.04*(34.09) | 0.25 ± 0.03*(24.24) |
| HAE 300 mg/kg | 0.28 ± 0.03*(28.21) | 0.24 ± 0.05*(45.45) | 0.22 ± 0.05*(33.33) |
| HAE 600 mg/kg | 0.31 ± 0.02*(20.51) | 0.24 ± 0.03*(45.45) | 0.22 ± 0.03*(33.33) |
*p < 0.05 compared with 5% Tween-20 treated group; HAE:
At 3 h post treatment the ASA, HAE 150, 300 and 600 mg/kg caused 35.29%, 29.41%, 32.94% and 31.76% reduction in paw volume in treated rats, respectively when compared with the negative control. The percentage inhibition in paw volume of HAE (300 and 600 mg/kg) treated groups were not significant (p > 0.05) compared to ASA treated group (
Egg albumin- induced paw edema
| Treatment (n = 6) | Mean increase in paw volume in ml ± SEM (% inhibition) | ||
|---|---|---|---|
| 1 h | 2 h | 3 h | |
| 5% Tween-20, 10 ml/kg | 0.85 ± 0.07 (-) | 0.83 ± 0.08 (-) | 0.85 ± 0.05 (-) |
| ASA 200 mg/kg | 0.83 ± 0.02 (2.35) | 0.78 ± 0.05 (6.02) | 0.55 ± 0.08*(35.29) |
| HAE 150 mg/kg | 0.93 ± 0.01 (-9.41) | 0.79 ± 0.02 (4.82) | 0.60 ± 0.04*(29.41) |
| HAE 300 mg/kg | 0.50 ± 0.03* (41.17) | 0.78 ± 0.06 (6.02) | 0.57 ± 0.09*(32.94) |
| HAE 600 mg/kg | 0.75 ± 0.08 (11.76) | 0.67 ± 0.09 (19.28) | 0.58 ± 0.07*(31.76) |
*p < 0.05 compared with 5% Tween-20 treated group; HAE:
The ASA and HAE 150, 300 and 600 mg/kg caused 67.89%, 9.17%, 19.27% and 35.78% reduction in writhing reflex in treated groups, respectively when compared with the negative control group (
Acetic acid induced writhing test
| Treatment (n = 6) | Mean writhing number | % inhibition |
|---|---|---|
| 5% Tween-20, 10 ml/kg | 21.80 ± 0.48 | - |
| ASA 200 mg/kg | 7.00 ± 0.58* | 67.89 |
| HAE 150 mg/kg | 19.80 ± 0.87* | 9.17 |
| HAE 300 mg/kg | 17.60 ± 0.66* | 19.27 |
| HAE 600 mg/kg | 14.00 ± 0.58* | 35.78 |
*p < 0.05 compared with 5% Tween-20 treated group; HAE:
Pentazocine and (HAE 150, 300 and 600 mg/kg) increased the PRT in treated rats by 67.62%, 19.05%, 35.24% and 22.86%, respectively when compared with the negative control. The PRT of HAE treated groups were low (p < 0.05) when compared to the pentazocine treated group (
Tail flick test
| Treatment (n = 6) | PRT (sec) | % inhibition |
|---|---|---|
| 5% tween-20, 10 ml/kg | 2.10 ± 0.21 | - |
| Pentazocine 3 mg/kg | 3.52 ± 0.41* | 67.62 |
| HAE 150 mg/kg | 2.50 ± 0.08* | 19.05 |
| HAE 300 mg/kg | 2.84 ± 0.24* | 35.24 |
| HAE 600 mg/kg | 2.58 ± 0.15* | 22.86 |
*p < 0.05 compared with 5% Tween-20 treated group; HAE:
The HAE reduced (p < 0.05) paw edema induced with formalin and egg-albumin and reduced (p < 0.05) writhing reflex in treated rat. It also increased the pain reaction time in treated rats. It produced potent anti-inflammatory and analgesic activities which might be linked to the phytoconstituents. Onoja and Anaga (17) reported the presence of flavonoids, Tannins, alkaloids and saponins in the methanol extract of
The formalin- and egg-albumin induced paw edema were used as the inflammatory models while acetic acid-induced writhing and tail flick test were used as the analgesic models (21). The HAE exhibited its optimum pharmacological activities at 300 mg/kg (Tables 1, 2, 3 and 4) as an increase in dose beyond 300 mg/kg did not produce any appreciable increase in the magnitude of the activities. This might be due to receptor site saturation and inhibition (16). The HAE is a mixture of bioactive compounds that may have diverse pharmacological activities (12).
The mechanism of the analgesic and anti-inflammatory activities may be the inhibition of cyclooxygenase (COX) activity; same mechanism of ASA. ASA irreversibly inhibit the cyclooxygenase which catalyze prostaglandin production from arachidonic acid (22-24). Prostaglandins are pro-inflammatory mediators (25, 26). The production of prostaglandins are controlled by the level of COX(s) activity and also influenced by the relative cell-specific expression of the terminal synthases, some of which may be co-induced with COX-2 (27, 28).
The HAE demonstrated analgesic activity against both central and peripheral pain. The acetic acid-induced writhing is sensitive and useful in the screening of centrally and peripherally acting drugs while the tail flick test is used in the screening of centrally acting drugs (20). Another possible mechanism of the analgesic activity may be desensitization of the nociceptor and/or increase in the pain threshold in the hypothalamus (22).
In conclusion, the study affirms the folkloric uses of