The protective effect of Ginsenoside Rg1 on aging mouse pancreas damage induced by D-galactose

Abstract

The protective effect and mechanism of Ginsenoside Rg1 on aging mouse pancreas damaged by D-galactose (D-gal)-induced was studied. Two-month-old male C57BL/6J mice were randomly divided into three groups of 10 mice per group. The D-gal group of mice received hypodermic injection of D-gal (120 mg/kg/day) for 42 days; the Rg1+D-gal group of mice receiving D-gal + intraperitoneal injection Rg1 (40 mg/kg/day) for 27 days from the 16th day of D-gal replication; and the naïve group that constituted the normal control mice receiving the same dose of saline instead of the drug. The related indicators were tested on the second day after modeling and administration. Fasting blood glucose (FBG), oral glucose tolerance test (OGTT) and fasting insulin level were measured by taking peripheral blood. Samples of pancreas were weighed and visceral index was calculated. Paraffin sections were prepared. H&E staining sections were produced to observe pancreatic tissue morphology. Immunohistochemical staining was used to observe advanced glycation end products (AGEs) and integral optical density (IOD) of stained positive tissue in pancreas. Ultrathin slices were used to observe ultrastructural change of pancreatic tissue. Frozen sections were prepared to test the relative optical density of positive cells that were stained by senescence-associated β-galactosidase (SA-β-gal) in pancreatic tissue. Superoxide dismutase (SOD), malonaldehyde (MDA) and total antioxidant capacity (T-AOC) were detected by preparing pancreas tissue homogenates. Compared with the control group, Rg1+D-gal mice had significantly decreased pancreatic wet weight and visceral index and significantly lower FBG; OGTT for 30 and 120 min. There was no significant difference of the blood sugar level between the groups. The area under the curve and the number and size of the nucleated cells within islet were markedly reduced. In addition, SA-β-gal-positive particles in pancreas tissue intracytoplasmic cells significantly decreased and relative optical density also reduced. The IOD of AGEs in pancreas tissue and MDA content decreased. SOD and T-AOC activity significantly increased. Ginsenoside Rg1 can be effective antagonistic structure and function of the pancreas injury induced by D-gal. The mechanism may be associated with reducing oxidative damage.

Ginsenoside Rg1 ameliorates testicular�senescence�changes in D‑gal‑induced aging mice via anti‑inflammatory and antioxidative mechanisms

“…There were no complications detected in any of the mice. In previous studies, complications were not identified in other organs ( 4 , 5 , 11 , 12 ).…”

Quercetin Attenuates Pancreatic and Renal D-Galactose-Induced Aging-Related Oxidative Alterations in Rats

“…In contrast, the Bcl2 gene and Bcl2 protein content in the pancreas were significantly decreased due to the enhancement of oxidative stress and decline of the antioxidant SOD1 gene. Similarly, Dong et al [ 24 ] stated a significant reduction in the pancreatic antioxidant potential in D-gal-treated mice via a significant decrease in SOD activity and total antioxidant capacity. On the other hand, malondialdehyde (MDA) contents in the pancreatic homogenate were significantly increased, indicating the oxidative alterations due to D-gal.…”

“…Yu et al [ 23 ] determined significant increases in brain IL-6 and NF-κB in D-gal-treated mice. Hypodermic injection of D-gal in mice significantly increased the relative optical density of positive cells that were stained with senescence-associated β-galactosidase (SA-β-gal) as an aging marker in pancreatic tissue [ 24 ]. Moreover, numerous oxidative effects have been found through significant increases in p21 expression [ 25 ] and IL-6 protein levels [ 26 ] in mice and Bcl2 protein immunostaining in rats [ 27 ].…”

Ameliorative effect of urolithin A ond-gal-induced liver and kidney damage in aging miceviaits antioxidative, anti-inflammatory and antiapoptotic properties

“…1 Accumulating evidence has shown that aging is one of the greatest risk factors leading to the dysfunction of normal cellular modulation, and aging is associated with numerous diseases, including diabetes, cancers, cardiovascular and cerebrovascular diseases (CCD), Alzheimer's disease (AD) and others, which are harmful to the health of aged people. 2,3 Thus, anti-aging has become one of the hot research topics with an increasing elderly population worldwide.…”