When a Gastric ulcer occurs in the stomach, it is called a gastric ulcer. The bacterium called H. pylori cause this type of ulcer. Antacids are used as a treatment option for gastric ulcers; the patient usually starts to feel well after two or three weeks of using antacids. Also, ulcer patients are advised not to use too much oily and greasy food and also asked to limit the consumption of acidic foods [12, 20, 21].

When a Gastric ulcer is in the duodenum, it is called a duodenal ulcer. The initial section of the small intestine is where this kind of gastric ulcer forms. Interesting contrasts exist between some duodenal ulcer symptoms and those of stomach ulcers. In the Western world, duodenal ulcers are the most typical kind of ulcers. [12, 20, 22].

Esophageal ulcers are lesions that occur in the esophagus (food pipe). These are most commonly formed at the end of the food pipe and can be felt as a pain right below the breastbone, in the same area where symptoms of heartburn are felt. Oesophageal ulcers are associated with acid reflux or GERD, prolonged use of drugs like NSAIDs and smoking [20, 23].

Internal bleeding is caused by a Gastric ulcer that has been left untreated. When this happens, it is referred to as a bleeding ulcer, this is the most dangerous type of ulcer and it requires immediate treatment [20, 24, 25].

Simple Gastric ulcers that have not healed after at least 3 months of treatment are called refractory ulcers [20].

A series of lesions (or lacerations) known as stress ulcers can develop in the esophagus, stomach, or duodenum. These are typically only seen in people who are seriously unwell or under a lot of stress [20, 25-27].

H. pylori is typically spread from person to person via saliva and faecal contamination of food or water. Untreated water, congested living circumstances, and inadequate hygiene all lead to higher H. pylori prevalence in poorer nations. The majority of persons become infected as youngsters, and parents and siblings appear to play a significant role in transmission [29, 32-34].

H. pylori enter the body through the mouth, moves through the digestive system, and infects the stomach or the first part of the small intestine. The spiral-shaped bacterium uses its tail-like flagella to move around and burrow into the stomach lining, which causes inflammation [32, 35]. Unlike other bacteria, H. pylori bacteria can survive in the stomach's harsh acidic environment because they produce a substance that neutralizes stomach acid. This substance, Urease, reacts with urea to form ammonia, which is toxic to human cells. Depending on where the infection occurs in the stomach, H. pylori can also cause the overproduction of stomach acid [32, 36, 37].

NSAIDs (Non-steroidal anti-inflammatory drugs): Nonsteroidal anti-inflammatory medications (NSAIDs) are the most well-known pharmaceuticals for the treatment of pain, inflammation, and fever globally. NSAIDs are often used to treat inflammatory conditions such as rheumatoid arthritis, osteoarthritis, dysmenorrhea, and ischemic cerebrovascular disorders. The use of these medications in some types of cancer treatment has also lately been documented. These medications work by inhibiting prostaglandin biosynthesis and thereby producing a therapeutic effect. On the other hand, long-term use of NSAIDs causes unpleasant gastrointestinal (GI) symptoms such as mucosal lesions, bleeding, gastric ulcer, and inflammation in the intestine leading to perforation, strictures in the small and large intestines, and chronic difficulties. Some of the side effects of NSAIDs may be transitory, but there have been numerous reports of life-threatening situations [36, 38, 39].

NSAIDs include Ibuprofen, Fenoprofen, Aspirin, Diclofenac, Sulindac, Naproxen, Indomethacin, Tolmetin and many others. These are valuable therapeutics that act not only as an anti-inflammatory but also as analgesics and antipyretics. They are used in a wide variety of clinical conditions, including arthritis and other musculoskeletal disorders. Nearly 25% of chronic users of these drugs develop gastric ulcer disease. Various studies indicate that NSAIDs help in the progression of ulceration by overcoming the expression of the enzyme cyclooxygenase (COX), which has been documented to inhibit the conversion of Arachidonic acid to PG’s that impairs the mucosal barrier and results in corrosive action with pepsin and results in the progression of Gastric ulcer [38, 40, 41]. Further, COX-1 inhibition by the NSAIDs leads to the significant release of endothelin-1 (ET-1), which is a potent vasoconstriction that has been shown to induce mucosal injury. NSAIDs, by inhibiting the prostaglandin synthesis, cause the activation of neutrophils and the local release of reactive oxygen species (ROS), thus initiating the gastric injury [40, 42, 43]. NSAIDs also cause a marked reduction in mucosal blood flow, mucus-bicarbonate secretions, impaired platelet aggregation, reduced epithelial cell renewal and increased leukocyte adherence, which are responsible for the pathogenesis of ulceration. Gastric acid worsens the NSAID effects by deepening superficial lesions interfering with platelet aggregation and impairing the ulcer healing process [40, 42, 44].

Mechanism of action of NSAIDs: The principle of action of nonsteroidal anti-inflammatory drugs (NSAIDs) was initially established in the early 1970s and is based on the inhibition of prostaglandin (PG) synthesis.PG, which is synthesised from arachidonic acid, is a major mediator of inflammation, pain, and fever. The enzyme cyclooxygenase (COX), also known as PGH synthase, catalyses the reaction. By binding to and inhibiting COX, NSAIDs prevent the PG production [45-47].COX has two isoforms, COX-1 and COX-2, each with a distinct function. COX-1 is expressed constitutively and responsible for the stomach mucosa's normal physiological protection. It is in charge of the manufacture of prostaglandins, which protect the stomach lining from acid secretion, keep blood flowing in the gastric mucosa, and create bicarbonate. COX-2, the other isoform, is activated by cell injury, proinflammatory cytokines, and tumor-derived substances. NSAIDs primarily cause NSAID-induced gastropathy by inhibiting COX-1 [45, 46, 48].NSAIDs are also directly cytotoxic to stomach mucosal cells, causing lesions and damage. One study discovered that direct cytotoxicity is unaffected by COX inhibition. This type of topical damage has been reported in the case of acidic NSAIDs such as aspirin, resulting in an accumulation of ionised NSAID, a phenomenon known as "ion trapping." NSAIDs are thought to produce membrane permeabilization, which disrupts the epithelial barrier. NSAIDs could also cause necrosis and apoptosis in gastric mucosal cells [49-51].