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Life Sci. 2019 Aug 5:116732. doi: 10.1016/j.lfs.2019.116732. [Epub ahead of print]

Linderane protects pancreatic β cells from streptozotocin (STZ)-induced oxidative damage.

Author information

1
The Second Department of Endocrinology, The First Hospital of Qiqihar, Qiqihar 161005, Heilongjiang Province, China; The Second Department of Endocrinology, Affiliated Qiqihar Hospital of Southern Medical University, Qiqihar 161005, Heilongjiang Province, China. Electronic address: zhang_haijun3@126.com.
2
Department of Cardiac Function, The First Hospital of Qiqihar, Qiqihar 161005, Heilongjiang Province, China; Department of Cardiac Function, Affiliated Qiqihar Hospital of Southern Medical University, Qiqihar 161005, Heilongjiang Province, China.
3
The Second Department of Endocrinology, The First Hospital of Qiqihar, Qiqihar 161005, Heilongjiang Province, China; The Second Department of Endocrinology, Affiliated Qiqihar Hospital of Southern Medical University, Qiqihar 161005, Heilongjiang Province, China.

Abstract

AIMS:

Linderane, an important bioactive compound in Linderae, improved glucose and lipid metabolism in ob/ob mice. However, the effect of linderane on streptozotocin (STZ)-induced oxidative damage in INS-1 cells remains unclear.

MAIN METHODS:

INS-1 cells were pre-treated with different doses of linderane for 2 h and then treated with 3 mM STZ for 12 h. Cell viability was determined by MTT assay. Cell apoptosis was detected using an Annexin V-FITC Apoptosis Detection Kit. The level of intracellular ROS was determined using dichlorofluorescein-diacetate (DCFH-DA). The activities of insulin secretion, SOD, catalase (CAT) and GPx were measured using ELISA kits. The expression levels of bax, bcl-2, p38, p-p38, nuclear Nrf2 and HO-1 were measured using western blot.

KEY FINDINGS:

The results showed that STZ-caused inhibitory effects on cell viability and insulin secretion were mitigated by linderane. Furthermore, linderane inhibited apoptosis and oxidative stress in STZ-induced INS-1 cells. Finally, linderane suppressed the activation of p38 MAPK pathway, as well as enhanced the activation of Nrf2 pathway in STZ-induced INS-1 cells. Activation of p38 MAPK pathway or inhibition of Nrf2 significantly reversed the protective effects of linderane against STZ-induced ROS production and cell apoptosis.

SIGNIFICANCE:

The protective effects of linderane on STZ-induced INS-1 cells might be attributed to the inhibition of p38 MAPK and activation of Nrf2 pathway.

KEYWORDS:

Diabetes mellitus (DM); Linderane; Nrf2 signaling pathway; Oxidative stress; Pancreatic islet β cells; p38 MAPK signaling pathway

PMID:
31394125
DOI:
10.1016/j.lfs.2019.116732

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