Neuroprotective effects of folic acid on experimental diabetic peripheral neuropathy

Abstract

Diabetic peripheral neuropathy (DPN) is widely considered as a degenerative complication of diabetic patients. The clinical effectiveness of folic acid (FA) on DPN is uncertain. The objective of the present study was to determine the effect of FA in DPN using electromyography (EMG), histopathological examination, immunohistochemistry, inclined plane test, and malondialdehyde (MDA) levels as a marker for lipid peroxidation in experimental diabetic rats. A total of 21 Sprague Dawley rats were randomly divided into 3 groups: control group, diabetes group, and FA-treated group. In EMG, compound muscle action potential (CMAP) amplitude in the sciatic nerve was lower in the diabetes group compared with the control group. CMAP amplitude in the sciatic nerve was higher in the FA-treated group when compared with the diabetes group. Distal latency and CMAP duration in the sciatic nerve were lower in the FA-treated group when compared with the diabetes group. In histopathological examination of the sciatic nerve, peripheral fibrosis was present in the diabetic group; the fibrosis was lower in the FA-treated group. In comparison with the diabetes group, the expression of nerve growth factor (NGF) was higher in the FA-treated group. The scores for the inclined plane test were lower in the diabetes group and higher in the FA-treated group than the control group. The MDA levels were significantly lower in the FA-treated group when compared with the diabetes group.The study suggests that FA can protect diabetic rats against DPN and that the underlying mechanism for this may be related to improvement of the expression of NGF and lower MDA levels.

Nutritional management of patients with diabetic peripheral neuropathy with L-methylfolate-methylcobalamin-pyridoxal-5-phosphate: results of a real-world patient experience trial

“…12 In an experimental model of DPN, folic acid protected against DPN, which was related to neuroprotective effects of folic acid. 17 Research on methylcobalamin (MC), the active form of vitamin B12, found that MC improved the somatic and autonomic symptoms of diabetic neuropathy among DPN patients (without causing side effects), 18 enhanced nerve regeneration in rats with DPN, 19 and delayed onset of DPN in rats. 20 An in vitro study showed that pyridoxine (P), the active form of vitamin B6, along with pyridoxamine (PM) were found to inhibit superoxide radical production, reduce lipid peroxidation and glycosylation, and increase the (Na + + K + )-ATPase activity in high glucose-exposed red blood cells (RBC) -suggesting P or PM supplementation may delay or inhibit DPN.…”

Effect of low‐level 1800 MHz radiofrequency radiation on the rat sciatic nerve and the protective role of paricalcitol

“…In our study, we observed the lowest g‐ratio in the RF group and there was a significant difference among the RF group and other groups. Previous studies reported that the prolongation in CMAP latency was due to increased myelin sheath thickness caused by edematous swelling, delamination, and rarefaction in the myelin sheath [Cankayali et al, ; Yilmaz et al, ]. We also thought that the decrease in CMAP amplitude was due to the decreased g‐ratio caused by axonal loss and increase of myelin sheath thickness.…”

Rat Bone Marrow-Derived Mononuclear Cells Outperform Folic Acid in the Treatment of Diabetic Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats

“…Group IV: (DA+FA): Diabetes-induced plus folic acid group; two weeks after the STZ injection, FA was injected intraperitoneally (10 mg/kg/day) for 4 weeks [5].…”

“…An increase in homocysteine levels or oxidative stress may be one of the possible mechanisms contribute to the development of DPN. A number of studies associated with FA deficiency and increased plasma total homocysteine levels show higher risk of vascular disease, cerebral ischemia, neuropsychiatric and neurodegenerative diseases [5]. Moreover, FA supplementation has been used to support a range of health concerns including DPN and provide neural protection in some neurological diseases [6].…”