Table 1.
Effect of Aspirin on various diseases.
| Diseases | Functions | Applications |
|---|---|---|
| Cardio-vascular diseases (152–160) | Controls cardiac hypertrophy and fibrosis by modulating angiotensin, thromboxane, and prostacyclin production, inhibits platelets activation and aggregation. Downregulates NF-κB, VCAM-1 and oxygen free radicals leading to reduction of vascular inflammation via p38MAPKs-NF-κB-VCAM-1 pathway. | Improves vascular dysfunction, cardiac hypertrophy, and oxidative stress. Reduces risk of non-fatal myocardial infarction. A low dose of aspirin may prevent from developing cardiovascular diseases, prevents second heart attack/stroke. Reduces stroke chances in diabetic patient with or without a history of heart disease. Prevents myocardial infarction and decreases incidence of stent thrombosis in patients with atrial fibrillation and atherosclerotic cardiovascular disease. |
| Thalassemia (161, 162) | Downregulates CD40L expression leading to reduction in inflammation and thrombosis in patient with thalassemia and β-thalassemia major. | Prevention of thrombosis and protect from new white matter brain lesions in beta thalassemia major patients. |
| Tumorigeneses of hepatic, ovarian and colon cancer (163–165) | Downregulates bcl-2 expression and upregulating Bax and p53 to inhibit tumorigenesis in lung, ovarian and colon cancer cells. Downregulates MMP-2 and E-cadherin expression along with platelet activation resulting in reduced invasion of hepatic adenocarcinoma cell line. | Reduces tumor growth and metastasis, inhibits tumor cell invasion. |
| Colorectal and colon cancers (166) | Inhibits WNT and MAPK pathways, arrest cell cycle. | Induces cancer cell apoptosis. |
| Hepatocellular carcinoma (167, 168) | Modulates NF-κB/P4HA2 axis and LMCD1-AS1/let-7g/P4HA2 axis in hepatocellular carcinoma. Induces high expression of DNA mismatch repair proteins hMLH1, hMSH2, hMSH6 and hPMS2. | Inhibits hepatocellular carcinoma. Inhibits cell cycle and induces apoptosis of human colon cancer cells. |
| Esophageal, prostate, breast, gastric, and gastro-intestinal cancers (153, 169–173) | Downregulates atherothrombosis, inactivates platelet aggregation and cancer metastasis in esophageal and gastro-intestinal cancers. Inhibits angiogenesis in gastric cancer. Enhances nitric oxide production leading to IKKβ-mediated inhibition of NF-κB activity in gastric, prostate and breast cancer stem cells. | Reduces risk of esophageal, gastric, breast, prostate, and gastro-intestinal cancers. |
| Bone degeneration (174) | Activation of osteoblastic bone formation and inhibition of osteoclast activities via cyclooxygenase-independent via Wnt/β-catenin pathways. | Maintaining bone mass, qualities, bone self-regeneration, and fracture-healing. |
| Non-alcoholic fatty liver disease (175) | Inhibits lipid biosynthesis, decreases levels of TNF-α and angiotensin II type1 receptor along with activation of PPARδ-AMPK-PGC-1α pathway, as well as by modulating the mannose receptor and C-C chemokine receptor type 2 levels in macrophages. | Improves non-alcoholic fatty liver disease and atherosclerosis. |