Fig. 8. Proposed mechanism of BPE as hepatoprotector and renoprotector in DM and Dyslipidemia rat model. In diabetic conditions, ROS in the body such as H₂O₂ are produced in excess. Normally this H₂O₂ can be overcome by the activity of the GPX enzyme to become H₂O through the oxidation of GSH to (Glutathione Disulfide) GSSG. However, the large number of H₂O₂ molecules disrupts the activity of the GSH-Px enzyme. On the other hand, other antioxidant enzymes, namely GST, can also convert GSH and xenobiotics, namely foreign substances that are not beneficial to the body, into safer Glutathione S-Conjugates. The presence of free radicals can also activate NFkB which causes the production of TNF-α which has an impact on inflammation. The presence of oxidative stress and inflammation in cells over time will develop into damage to organs such as the liver and kidneys. Liver damage is characterized by increased ALP enzymes, as well as decreased protein and albumin. In the kidney, inflammation and oxidative stress have an impact on decreasing the GFR which causes BUN, SCr, and UA in the blood cannot be excreted. Treatment with BPE can neutralize H₂O₂ in cells by increasing GSH-Px and GST enzyme activity, also downregulating NF-kB and TNF-a, as well as reducing the risk of liver damage by reducing ALP enzyme expression and increasing total protein and albumin. BPE also increases GFR so that BUN, SCr, and UA can be excreted properly.