Affiliations 

  • 1 UPM-MAKNA Cancer Research Laboratory, Institute of Bioscience, Universiti Putra Malaysia, 43400 UPM Serdang, Selangor Malaysia
  • 2 Faculty of Veterinary Medicine, Universiti Putra Malaysia, UPM, Serdang, Malaysia
J Diabetes Metab Disord, 2022 Jun;21(1):1-11.
PMID: 35673507 DOI: 10.1007/s40200-021-00905-0

Abstract

PURPOSE: Diabetes accelerates peripheral, distal symmetric polyneuropathy, small fiber predominant neuropathy, radiculoplexopathy, and autonomic neuropathy. This study investigated the neuroprotective effects of gallic acid and myricetin-rich Labisia pumila extract in a diabetic neuropathy rat model and evaluated the neuropathy correlationship with serum inflammatory biomarkers.

METHODS: Thirty male rats were divided into 5 groups (n = 6), namely: healthy control; non-treated diabetic control; and diabetic-rats treated with 200 mg/kg metformin; Labisia pumila ethanol extract (LP) at 150 mg/kg or 300 mg/kg doses. Diabetes was induced by 60 mg streptozotocin /kg intraperitoneal injection. Rats were orally treated daily for ten weeks. Their fasting blood glucose (FBG), neurological functions (hot plate and tail immersion; thermal hyperalgesia; cold allodynia; motor walking function), biomarkers for inflammation and oxidative stress, the neuro-histopathological changes, and brain somatic index were measured.

RESULTS: The extract significantly prevented abnormal increases in FBG and decreases in body weight gain. It attenuated behavioral dysfunctions (hot plate and tail immersion; thermal hyperalgesia; cold allodynia; motor walking function), systemic inflammation (serum TNF-α, prostaglandin-E2) oxidative tension (malondialdehyde), histological brain and sciatic nerve injuries in the diabetic-rats, better than Metformin.

CONCLUSION: LP mitigated neural dysfunction better than metformin partly by amending diabetic systemic inflammation, oxidative tension, and diabetic abnormalities. The nerve injuries were strongly correlated to serum prostaglandin-E2, TNF-α levels, and walking functions. The motor function was correlated to sensory neuronal functions, inflammation, and oxidation. The sensory neuronal functions were more affected by TNF-α than prostaglandin-E2 or oxidation. Diabetic brain and sciatic nerve deteriorations were influenced by serum TNF-α, PGE2, and MDA levels.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s40200-021-00905-0.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.