Let's say you're on the football field and sand gets in your eyes. How do you know there's sand there? Of course you can't see it, but if you're a normal, healthy person, you can feel it. Feeling of extreme discomfort, also known as pain. Well, the pain is forcing you to do something, in this case, rinse your eyes until the sand is gone. 

And how do you know the sand is gone? Yeah. Because there is no more pain. There are people who don't feel pain. Well, that might sound great, but it's not. If you can't feel pain, you could hurt yourself or even hurt yourself without knowing it. .Pain is your body's early warning system. It protects you from the world around you and from yourself. As we get older, we install pain detectors in most areas of our body. These detectors are specialized nerve cells called nociceptors that extend from your spinal cord to your skin,  muscles,  joints, teeth, and some of your internal organs.Like all nerve cells, they conduct electrical signals and send information  back to your brain from wherever they are. 


But unlike other neurons, nociceptors only fire when something happens that could or will cause damage. So gently touch the tip of a needle. You will feel the metal, and these are your normal nerve cells. But you won't feel any pain.The more you press against the needle, the closer you get to the nociceptor's threshold. Push hard enough and you'll cross that threshold and  nociceptors will fire, telling your body to stop  whatever it's doing. But pain The Threshold is not a setting stone. Certain chemicals can turn off nociceptors and lower your pain threshold.When cells are damaged, they and other nearby cells start spitting out these tuning chemicals like mad, lowering the nociceptor threshold to the point where a mere touch can cause pain. 


And that's where over-the-counter pain relievers come in. Aspirin and ibuprofen block the production of a class of these tuning chemicals called prostaglandins. Let's take a look at how they do it. When cells are damaged release, they free a chemical called arachidonic acid.


And two enzymes called COX1 and COX2 convert that arachidonic acid into prostaglandin H2, which is then converted into a variety of other chemicals that do many things, including raising body temperature, causing inflammation, and lowering pain thresholds. Now all enzymes have an active center. This is the part of the enzyme where the reaction takes place. The active sites of COX1 and COX2 are well matched to arachidonic acid. As you can see, there is no free space.Well, this is where aspirin and ibuprofen do their work. Therefore they work differently. Aspirin acts like a porcupine's spine. It enters the active side and then breaks off, leaving half of itself  there, completely blocking that channel. and arachidonic acid make it impossible  to pass.This permanently disables COX1 and COX2. Ibuprofen, on the other hand, penetrates the active site but is not broken down or altered by the enzyme. COX1 and COX2 can spit it out again, but by the time  ibuprofen is in it, the enzyme can't bind to arachidonic acid and carry out its normal chemistry. 


But how do aspirin and ibuprofen know where the pain is?Well they don't. Once the drugs enter the bloodstream, they are transported throughout the body, going to painful areas just like normal areas. This is how aspirin and ibuprofen work. But pain has other dimensions. .Neuropathic pain, for example, is pain caused by damage to our own nervous system; no external stimulus is required.And scientists are discovering that the brain controls how we respond to pain signals. For example, how much pain you feel can depend on whether you pay attention to the pain or even on your mood. Pain is an area of ​​active research. understand  better, maybe we can help people deal with it better.



Reference:


Cyclooxygenase?2 (COX?2) Is An Enzyme That Is Activated After An Injury.


Enzyme Active Site and Substrate Specificity


Mrs. Mazzuca's Honors Biology Blog


Nociceptors – Neuroscience– NCBI Bookshelf