Extract had ability to induce antioxidant Chlorhexidine hydrochloride enzymes in Nrf2-mediated fashion in the tissues as NQO1 is one of the typical antioxidant downstream to Nrf2 signaling pathway. While the constituents responsible for NQO1 induction in mouse tissues remain unclear, there is possibility that artemisinin and its derivatives played a role in the enzyme induction because artemisinin content in the sample was 1.6 mg/g that is enough to affect Nrf2 signaling. In addition, NQO1 antioxidant enzyme in tissues from mice fed Artemisia annua extract may be attributable to phenolic compounds such as flavonoids and coumarins that are electrophiles with antioxidant activity and hold capability to induce phase 2/ antioxidant enzymes through activating Nrf2 signaling pathway. In conclusion, AA extract showed antioxidative activity in hepatoma cells as well as protected from lipid peroxidation and DNA damage in D-galactose-induced oxidative stress mouse model. Therefore, it deserves further clinical study to be developed into health functional ingredient. Previous studies based on healthcare utilization data have reported an increased risk of type 2 diabetes in patients with RA. In contrast, our study showed that female patients with type 2 diabetes were associated with a significantly increased risk for incident RA. The increased risk of type 2 diabetes in patients with RA was proposed to be due to the long-term use of steroids during RA treatment. Nevertheless, a Canadian study using a population-based health insurance 4-(Benzyloxy)phenol database demonstrated a similar risk of incident type 2 diabetes in patients with RA, with or without adjusting for the use of oral or topical glucocorticoids. Conversely, decreased insulin sensitivity was reported in patients with RA upon long-term exposure to steroids. Thus, the role of long-term steroid use among patients with RA in the development of type 2 diabetes still requires further investigation. Furthermore, lifestyle changes after diagnosis of RAmight also contribute to an increase in the risk of developing type 2 diabetes. One health insurance database study performed in the United Kingdom concluded that the observed association between patients with RA and incident type 2 diabetes could substantially explained by obesity and lifestyle factors. Our findings also showed that the risks between type 2 diabetes and incident RA were more prominent in younger female patients and in those with a shorter interval between the diagnosis of type 2 diabetes and RA. In the youngest age group of 20 to 44 years, the risk of developing RA was 3.6 times higher in patients with type 2 diabetes compared with patients without type 2 diabetes. Since both RA and type 2 diabetes are primarily chronic diseases of an older population, a strong positive association in young female patients is of concern. It is possible that these patients are genetically susceptible for developing autoimmune diseases, which tends to manifest early in life. Furthermore, the association between type 2 diabetes and incident RA was found to be strongest for patients with the shortest time intervalbetween the diagnosis of type 2 diabetes and the index date. Conversely, patients whose RA appeared 11 years or more after the diagnosis of type 2 diabetes were not significantly associated with the presence of type 2 diabetes. The proximity in the timing between when these two conditions occurred is consistent with the notion that type 2 diabetes and RA are related.