Allium hookeri root protects oxidative stress-induced inflammatory responses and β-cell damage in pancreas of streptozotocin-induced diabetic rats

Abstract

Background: Water extract from the root of Allium hookeri (AH) shows anti-inflammatory, antioxidant, and free radical scavenging effects. In this study, the ameliorating effects of AH on oxidative stress-induced inflammatory response and β-cell damage in the pancreas of streptozotocin (STZ)-induced type 1 diabetic rats were investigated.

Methods: AH (100 mg/kg body weight/day) was orally administered every day for 2 weeks to STZ-induced diabetic rats. After the final administration of AH, biochemical parameters including glucose, insulin, reactive oxygen species levels, and protein expressions related to antioxidant defense system in the pancreas of STZ-induced diabetic rats.

Results: The diabetic rats showed loss of body weight and increased pancreatic weight, while the oral administration of AH attenuated body and pancreatic weight changes. Moreover, the administration of AH caused a slightly decrease in the serum glucose level and a significant increase in the serum and pancreatic insulin levels in the diabetic rats. AH also significantly reduced the enhanced levels of reactive oxygen species, oxidative stress biomarker, in the serum and pancreas. The diabetic rats exhibited a down-regulation of the protein expression related to antioxidant defense system in the pancreas, but AH administration significantly up-regulated the expression of the heme oxygenase-1 (HO-1). Furthermore, AH treatment was reduced the overexpression of nuclear factor-kappa B (NF-кB)p65 and NF-кBp65-induced inflammatory cytokines such as tumor necrosis factor-α and interleukin-6. In addition, AH treatment was less pancreatic β-cell damaged compared with those of the diabetic rats.

Conclusion: These results provide important evidence that AH has a HO-1 activity on the oxidative stress conditions showing pancreato-protective effects against the development of inflammation in the diabetic rats. This study provides scientific evidence that AH protects the inflammatory responses by modulated NF-кBp65 signaling pathway through activation of HO-1 in the pancreas of STZ-induced diabetic rats.

Fig. 1

Identification of chemical ingredients of root extract of Allium hookeri

Fig. 2

Insulin expression in the pancreas. NC, non-diabetic control rats; DC, diabetic control rats; AH, Allium hookeri-treated diabetic rats. The results are presented as the mean ± SEM for five rats in each group. ^* P < 0.001 versus DC

Fig 3.

ROS content in the pancreas. NC, non-diabetic control rats; DC, diabetic control rats; AH, Allium hookeri-treated diabetic rats. The results are presented as the mean ± SEM for five rats in each group. ^* P < 0.001 versus DC

Fig. 4

Representative SOD, catalase, and HO-1 protein expressions in the pancreas. NC, non-diabetic control rats; DC, diabetic control rats; AH, Allium hookeri-treated diabetic rats. The results are presented as the mean ± SEM for five rats in each group. ^* P < 0.05, ^** P < 0.01 versus DC

Fig. 5

Representative NF-кBp65, TNF-α, and IL-6 protein expressions in the pancreas. NC, non-diabetic control rats; DC, diabetic control rats; AH, Allium hookeri-treated diabetic rats. The results are presented as the mean ± SEM for five rats in each group. ^* P < 0.05, ^** P < 0.01, ^*** P < 0.001 versus DC

Fig. 6

H/E staining of pancreatic tissue. a non-diabetic control rats, b diabetic control rats, c Allium hookeri-treated diabetic rats. Images are at × 400 magnification (n = 5)

Fig. 7

Predicted mechanism in pancreatic tissue on administering AH. Our study revealed that AHR suppresses STZ-induced type 1 diabetes. An important mechanism of AHR’s anti-diabetic effect is its capacity to reduce the oxidative stress state by diminishing ROS generation and lipid peroxidation in the pancreas. Our data further suggest that another critical mechanism of AHR’s anti-diabetic property is its ability to ameliorate inflammation through modulation of the serum TNF-α and IL-6 levels and the pancreatic protein expressions of NF-кB