## 2 Results and Discussions
### Antidiabetic Activity of Essential Oil and Isolated Compound (Osthole)  
The effect of the obtained essential oil and the pure compound (osthole) from _P. prabularia_ roots for its _in vitro_ inhibition of the enzyme PTP-1B was determined. The essential oil induced a PTP-1B enzymatic inhibition in a concentration-dependent manner with IC\({}_{50}\) values 0.06 \(\pm\) 0.01 ug/mL (_p_ \(<\) 0.02), which is more than 25 times more potent than the positive control (3-(3,5-dibromo-4-hydroxybenzoylyl)-2-ethylbenzofuran-6-sulfonic acid-(4-(thiazol-2-ylsulfonyl)-phenyl)-amide) with IC\({}_{50}\) 1.46 \(\pm\) 0.4 ug/mL (_p_ \(<\) 0.05). The individual compound (osthole) also exhibited strong inhibitory activity against PTP-1B, with IC\({}_{50}\) values 0.93 \(\pm\) 0.1 ug/mL (_p_ \(<\) 0.01); it was also more effective than the positive control. The dose response curves of the inhibition of the PTP-1B enzyme of _P. prabularia_ essential oil and osthole are shown in Figure 3.  
[PERSON] and co-authors presented a strategy based on GC-MS coupled with molecular docking for analysis, identification, and prediction of PTP-1B inhibitors in the Himalayan cedar essential oil. \(\beta\)-Pinene (49.3%), \(\alpha\)-pinene (29.4%), \(\alpha\)-terpineol (4.1%), and \(\beta\)-caryophyllene (3.7%) were the main components of Himalayan cedar oil that inhibited PTP-1B with IC\({}_{50}\) value 120.71 \(\pm\) 0.26 ug/mL. The docking results of the PTP-1B inhibitory activity of caryophyllene oxide was also in agreement with its _in vitro_ activity [46]. The IC\({}_{50}\) value for PTP-1B inhibition for caryophyllene oxide was in the range 25.8-31.3 uM [46; 47]. New terpened cordroodols A-B from _Cedrela odorata_ showed inhibitory PTP-1B activity with IC\({}_{50}\) values 13.09 and 3.93 ug/mL, respectively [48]. In another study, [PERSON] and co-authors reported the _in vivo_ antidiabetic activity of _Cymbopogon citratus_ essential oil with major compounds, gerani (42.4%), neral (29.8%), myrcene (8.9%), and geraniol (8.5%), which were fully supported by molecular docking predictions [49].  
[PERSON] investigated the hypoglycemic effects of osthole in diabetic db/db mice, and the main mechanisms of these effects were elucidated using an _in vitro_ cell-based assay and _in vivo_ assays using a diabetic db/db mouse model. Results showed that osthole significantly alleviated hyperglycemia by activating PPAR\(\alpha\)/\(\gamma\) in a dose-dependent manner based on the results of the transition transfection assay [50; 51]. [PERSON] reported that the western blot analysis revealed osthole to significantly induce phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) as well as increase translocation of glucose transporter 4 (GLUT4) to plasma membranes and glucose uptake in a dose-dependent manner [50]. These results suggest that the increase in the AMP:ATP ratio by osthole had triggered activation of the AMPK signaling pathway, leading to increases in plasma membrane GLUT4 concentration and glucose uptake level [52]. Other research has clearly shown that osthole lowered fasting blood glucose (FBG) and improved insulin secretion. This may indicate partial recovery from pancreatic damage, as indicated from histological characteristics [53].  
Figure 3: Dose response curve of inhibition of protein-tyrosine phosphatase 1B (PTP-1B) enzyme for _Prangos rubularia_ essential oil (**A**) (IC\({}_{50}\) = 0.06 \(\pm\) 0.01 ug/mL) and the pure compound osthole (**B**) (IC\({}_{50}\) = 0.93 \(\pm\) 0.01 ug/mL).