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

  • Life Sci. 2019 Sep 15:233:116732. doi: 10.1016/j.lfs.2019.116732.
Haijun Zhang  1 ,  Chunping Zhu  2 ,  Zhe Sun  3 ,  Xiaoguang Yan  3 ,  Huihui Wang  3 ,  Haibo Xu  3 ,  Jiani Ma  3 ,  Yanrong Zhang  3
Affiliations
  • 1. The Second Department of Endocrinology, The First Hospital of Qiqihar, Qiqihar 161005, Heilongjiang Province, China; The Second Department of Endocrinology, Affiliated Qiqihar Hospital, Southern Medical University, Qiqihar 161005, Heilongjiang Province, China. Electronic address: [email protected].
  • 2. Department of Cardiac Function, The First Hospital of Qiqihar, Qiqihar 161005, Heilongjiang Province, China; Department of Cardiac Function, Affiliated Qiqihar Hospital, 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, Southern Medical University, Qiqihar 161005, Heilongjiang Province, China.
PMID: 31394125 DOI: 10.1016/j.lfs.2019.116732
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.
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