Chlorogenic Acid Ameliorates Liver Function in Association with Bax Downregulation, P53 Downregulation and Bcl-2 Upregulation in Diabetic Wistar Rat

Abstract

Hyperglycemia in Diabetes mellitus (DM) induces oxidative stress and mitochondrial disruptions in the liver, thereby triggering apoptosis through Bcl-2 family signaling. Excessive apoptosis leads to liver dysfunction. Chlorogenic acid (CGA) was elucidated in this study in preventing liver dysfunction as a progression of DM. The diabetic model was conducted in Wistar rats, divided into six groups. Blood examinations were done to measure the levels of blood glucose, SGOT, and SGPT. The liver was harvested for analysis of SOD2, Bax, and Bcl-2 mRNA. A paraffin section was used for p53 immunostaining. Liver dysfunction occurred in the DM 2 months group indicated by higher levels of SGPT and SGOT, higher expression of Bax, and lower expression of Bcl-2 compared to the control group. Giving CGA 12.5 mg/kgBW ameliorated blood glucose and liver enzyme levels, which were associated with lower expression of Bax, lower signaling of p53, and higher expression of Bcl-2 compared to DM 2 months group. Administration of CGA did not affect SOD2 expression in diabetic rats. CGA may attenuate liver dysfunction in diabetic rats through downregulation of Bax and p53, and upregulation of Bcl-2 signaling.

Eucommia ulmoides Leaves Alleviate Cognitive Dysfunction in Dextran Sulfate Sodium (DSS)-Induced Colitis Mice through Regulating JNK/TLR4 Signaling Pathway

“…As a result, AEEL showed an improvement effect on apoptosis by downregulating the expression levels of apoptosisrelated factors and upregulating the expression levels of anti-apoptosis-related factors in DSS-induced mice (Figure 9). According to Setyaningsih et al (2022), chlorogenic acid inhibits apoptosis by decreasing the expression level of BAX and increasing the expression level of BCl-2 in streptozotocin (STZ)-induced rats [60]. Cheng et al (2022) reported that E. ulmoides extract inhibits apoptosis by downregulating the expression level of BAX and cleaved caspase 3 and upregulating the expression level of BCl-2 in spinal cord-injury rats [61].…”