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Effects and mechanism of Ganoderma lucidum polysaccharides in the treatment of diabetic nephropathy in streptozotocin-induced diabetic rats

  • Yu Hu
    ,
  • Shu-Xiang Wang
    ,
  • Fu-Yu Wu
    ,
  • Ke-Jia Wu
    ,
  • Rui-Ping Shi
    ,
  • Li-Hong Qin
  • Jiamusi University
    ,
  • Huzhou University
Research Output: Contribution to journal Article Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Ganoderma lucidum polysaccharides (GLP) have renal protection effect but there was no study on the diabetic nephropathy. This study was designed to investigate its effect and mechanism using a diabetic rat model induced by streptozotocin (50 mg/kg, i.p.). The diabetic rats were treated with GLP (300 mg/kg/day) for 10 weeks. The blood glucose, glycated hemoglobin, body weight, and the levels of blood creatinine, urea nitrogen, and urine protein were assessed. And renal pathologies were assessed by the tissue sections stained with hematoxylin-eosin, Masson’s trichome, and periodic acid-Schiff. The expression of phosphorylated phosphoinositide 3 kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), and phosphorylated mammalian target of rapamycin (p-mTOR), the autophagy proteins beclin-1, LC3-II, LC3-I, and P62; the apoptosis-related proteins caspase-3 and caspase-9; and the inflammation markers IL-6, IL-1β, and TNF-ɑ were assessed. Results showed that GLP alleviated the impairment of renal function by reducing urinary protein excretion and the blood creatinine level and ameliorated diabetic nephropathy. The expression of p-PI3K, p-Akt, and p-mTOR in the diabetic kidney were significantly reduced in the GLP treatment group compared to the without treatment group. GLP treatment activated the autophagy indicators of beclin-1 and the ratio of LC3-II/LC3-I but reduced p62 and also inhibited the expression of caspase-3, caspase-9 and IL-6, IL-1β, and TNF-ɑ. In conclusion, the effect of GLP amelioration diabetic nephropathy may be via the PI3k/Akt/mTOR signaling pathway by inhibition of the apoptosis and inflammation and activation of the autophagy process.

Publication Information

Output type

Research Output: Contribution to journal Article Peer-review

Original language

English

Article number

4314415

Journal (Volume, Issue Number)

BioMed Research International (Volume 2022, Issue 4314415)

Publication milestones

  • Accepted/In press - 07/01/2022
  • Published - 08/03/2022

Publication status

Published - 08/03/2022

ISSN

2314-6133

External Publication IDs

  • handle.net: 10547/625367
  • Scopus: 85126664291
  • PubMed: 35299891

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