Dear Bhawana,

In some cases, anti-inflammatory and analgesic activities may be linked with the presence of the anti-oxidant agents such as polyphenolic and/or flavonoidal compounds in the extract.  However, it is NOT a mandatory that analgesic and/or anti-inflammatory agents should possess antioxidant properties. The mechanism of action of many of the commercially available analgesic and anti-inflammatory agents is via routes that not involved any oxidation process. For example, the non-steroidal anti-inflammatory drugs (NSAIDs) exert their analgesic and anti-inflammatory effects via inhibiting the enzymes COX 1 and COX 2 and NOT via anti-oxidant activity.

I suggest that you characterize the compounds in each extract if possible and test their analgesic and anti-inflammatory effects.

Antioxidant activity is NOT always the right tool to predict analgesic or anti-inflammatory effect of a compound.

Hoping this will be helpful,

Rafik

Thanks Rafik Sir for your valuable suggestion. Sir in discussion part, then there is no need of writing any correlation between antioxidant activity and biological activity for n-hexane extract. 

Rafik Sir  if you are having any research article regarding the above discussion please Sir can you share it. It will be a great help from your side.

Dear Bhawana,

Non-steroidal anti-inflammatory drugs

Non-steroidal anti-inflammatory drugs (NSAIDs) alleviate pain by counteracting the cyclooxygenase (COX) enzyme. On its own, COX enzyme synthesizes prostaglandins, creating inflammation. In whole, the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the pain. Some common examples of NSAIDs are aspirin, ibuprofen, and naproxen. The newer specific COX-inhibitors are not classified together with the traditional NSAIDs even though they presumably share the same mode of action. On the other hand, there are analgesics that are commonly associated with anti-inflammatory drugs but that have no anti-inflammatory effects. An example is paracetamol(known as acetaminophen in the U.S). As opposed to NSAIDs, which reduce pain and inflammation by inhibiting COX enzymes, paracetamol has - as early as 2006 - been shown to block the reuptake of endocannabinoids, which only reduces pain, likely explaining why it has minimal effect on inflammation.

References:

Ottani, Alessandra; Leone, Sheila; Sandrini, Maurizio; Ferrari, Anna; Bertolini, Alfio (February 15, 2006). "The analgesic activity of paracetamol is prevented by the blockade of cannabinoid CB1 receptors". European Journal of Pharmacology. 531 (1-3): 280–281. doi:10.1016/j.ejphar.2005.12.015. PMID 16438952.

Dani, Mélina; Guindon, Josée; Lambert, Chantal; Beaulieu, Pierre (November 14, 2007). "The local antinociceptive effects of paracetamol in neuropathic pain are mediated by cannabinoid receptors". European Journal of Pharmacology. 573 (1-3): 214–215. doi:10.1016/j.ejphar.2007.07.012. PMID 17651722

The mechanisms of action of NSAIDs in analgesia

Traditionally, the analgesic action of nonsteroidal anti-inflammatory drugs (NSAIDs) has been explained on the basis of their inhibition of the enzymes that synthesise prostaglandins. However, it is clear that NSAIDs exert their analgesic effect not only through peripheral inhibition of prostaglandin synthesis but also through a variety of other peripheral and central mechanisms. It is now known that there are 2 structurally distinct forms of the cyclo-oxygenase enzyme (COX-1 and COX-2). COX-1 is a constitutive member of normal cells and COX-2 is induced in inflammatory cells. Inhibition of COX-2 activity represent the most likely mechanism of action for NSAID-mediated analgesia, while the ratio of inhibition of COX-1 to COX-2 by NSAIDs should determine the likelihood of adverse effects. In addition, some NSAIDs inhibit the lipoxygenase pathway, which may itself result in the production of algogenic metabolites. Interference with G-protein-mediated signal transduction by NSAIDs may form the basis of an analgesic mechanism unrelated to inhibition of prostaglandin synthesis. These is increasing evidence that NSAIDs have a central mechanism of action that augments the peripheral mechanism. This effect may be the result of interference with the formation of prostaglandins within the CNS. Alternatively, the central action may be mediated by endogenous opioid peptides or blockade of the release of serotonin (5-hydroxytryptamine; 5-HT). A mechanism involving inhibition of excitatory amino acids of N-methyl-D-aspartate receptor activation has also been proposed.

As I have mentioned before there is no correlation between anti-oxidant activity (property) of an extract and analgesic and anti-inflammatory activities.

For example, ascorbic acid (vitamin C) is a good anti-oxidant, however, it does not have any analgesic or anti-inflammatory effect.

Another example, ibuprofen is an analgesic and anti-inflammatory agent but does not possess any anti-oxidant activity.

I have not found any report in the literature that quantitatively correlate anti-oxidant property to these two kinds of activity.

Hoping this clarifies my point,

Rafik

thanks dear Rafik Sir for your valuable suggestions and thanks for providing me references