Beneficial effects of ferulic acid alone and in combination with insulin in streptozotocin induced diabetic neuropathy in Sprague Dawley rats

Dhaliwal, Jatinder; Dhaliwal, Navneet; Akhtar, Ansab; Kuhad, Anurag; Chopra, Kanwaljit

doi:10.1016/j.lfs.2020.117856

Cited by 31 publications

(9 citation statements)

References 59 publications

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“… 28 Accordingly, the treatment of diabetic rats with insulin or antioxidants is associated with improved nerve function. 29 Therefore, the potential neuroprotective role of albumin may be related to its antioxidant properties.…”

Section: Discussionmentioning

confidence: 99%

Association Between Serum Albumin Levels and Diabetic Peripheral Neuropathy Among Patients with Type 2 Diabetes: Effect Modification of Body Mass Index

Hu¹,

Wang²,

Zeng³

et al. 2022

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Background The role of serum albumin in the risk of diabetic peripheral neuropathy (DPN) remains unclear. This study aimed to explore the relationship between serum albumin level and DPN, and to examine any possible effect modifiers among patients with type 2 diabetes mellitus. Methods This cross-sectional study was conducted in Jiangxi, China, from May 2012 to December 2014. Serum albumin levels were determined in 523 subjects, and the association between serum albumin level and DPN was evaluated using linear regression models (odds ratio [OR] and corresponding 95% confidence interval [CI]). Results There was a significant inverse association between serum albumin level (per 1 g/L increment, OR 0.95 [95% CI 0.92–0.98]) and the risk of DPN. Accordingly, when serum albumin was assessed as quartiles, a significantly lower risk of DPN was found in participants in quartile 4 (OR 0.49 [95% CI 0.25–0.95]), compared with those in quartile 1. Consistently, higher albumin levels (≥35 g/L) were associated with decreased odds for DPN (OR 0.36 [95% CI 0.17–0.74]) compared with lower levels. Furthermore, the albumin–DPN association was significantly stronger in patients with a relatively high body mass index (BMI; ≥24 kg/m 2 ; OR 0.91 [95% CI 0.85–0.98]) than in those with a low BMI (<24 kg/m 2 ; OR 0.99 [95% CI 0.94–1.04]; P for interaction = 0.042). Conclusion These data suggest that serum albumin level could be a novel risk factor for DPN among patients with type 2 diabetes and relatively high BMI (>24 kg/m 2 ).

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Section: Discussionmentioning

confidence: 99%

Association Between Serum Albumin Levels and Diabetic Peripheral Neuropathy Among Patients with Type 2 Diabetes: Effect Modification of Body Mass Index

Hu¹,

Wang²,

Zeng³

et al. 2022

DMSO

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“…Ferulic acid exhibits a potential advantage in the treatment of sciatica. Ferulic acid can decrease the levels of oxidative stress, inflammation and apoptosis markers in the sciatic nerves of patients with diabetes 12 . Ferulic acid exerts a neuroprotective effect against radiation‐induced nerve damage by targeting the NLRP3 inflammasome to enhance learning and memory ability and ameliorate pathological changes in the hippocampal tissues of irradiated mice 13 .…”

Section: Introductionmentioning

confidence: 99%

Ferulic acid alleviates sciatica by inhibiting neuroinflammation and promoting nerve repair via the TLR4/NF‐κB pathway

et al. 2023

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Introduction Sciatica causes intense pain. No satisfactory therapeutic drugs exist to treat sciatica. This study aimed to probe the potential mechanism of ferulic acid in sciatica treatment. Methods Thirty‐two SD rats were randomly divided into 4 groups: sham operation, chronic constriction injury (CCI), mecobalamin, and ferulic acid. We conducted RNA sequencing, behavioral tests, ELISA, PCR, western blotting, and immunofluorescence analysis. TAK‐242 and JSH23 were administered to RSC96 and GMI‐R1 cells to explore whether ferulic acid can inhibit apoptosis and alleviate inflammation. Results RNA sequencing showed that TLR4/NF‐κB pathway is involved in the mechanism of sciatica. CCI induced cold and mechanical hyperalgesia; destroyed the sciatic nerve structure; increased IL‐1β, IL‐6, TNF‐α, IL‐8, and TGF‐β protein levels and IL‐1β, IL‐6, TNF‐α, TGF‐β, TLR4, and IBA‐1 mRNA levels; and decreased IL‐10 and INF‐γ protein levels and IL‐4 mRNA levels. Immunohistochemistry showed that IBA‐1, CD32, IL‐1β, iNOS, nNOS, COX2, and TLR4 expression was increased while S100β and Arg‐1 decreased. CCI increased TLR4, IBA‐1, IL‐1β, iNOS, Myd88, p‐NF‐κB, and p‐p38MAPK protein levels. Treatment with mecobalamin and ferulic acid reversed these trends. Lipopolysaccharide (LPS) induced RSC96 cell apoptosis by reducing Bcl‐2 and Bcl‐xl protein and mRNA levels and increasing Bax and Bad mRNA and IL‐1β, TLR4, Myd88, p‐NF‐κB, and p‐p38MAPK protein levels, while ferulic acid inhibited cell apoptosis by decreasing IL‐1β, TLR4, Myd88, p‐NF‐κB, and p‐p38MAPK levels and increasing Bcl‐2 and Bcl‐xl levels. In GMI‐R1 cells, Ferulic acid attenuated LPS‐induced M1 polarization by decreasing the M1 polarization markers IL‐1β, IL‐6, iNOS, and CD32 and increasing the M2 polarization markers CD206, IL‐4, IL‐10 and Arg‐1. After LPS treatment, IL‐1β, iNOS, TLR4, Myd88, p‐p38MAPK, and p‐NF‐κB levels were obviously increased, and Arg‐1 expression was reduced, while ferulic acid reversed these changes. Conclusion Ferulic acid can promote injured sciatic nerve repair by reducing neuronal cell apoptosis and inflammatory infiltration though the TLR4/NF‐κB pathway.

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“…These findings suggest that FA attenuates cognitive impairment in rat model of diabetes mellitus by regulating protein-tyrosine phosphatase 1B and insulin signaling pathway [111]. In addition to monotherapy, insulin-FA combination therapy improved peripheral nerve function in diabetic rats via enhancing glycemic control and suppressing inflammatory and apoptotic markers [112]. When tested in high fat-induced obesity, FA treatment decreased hepatic lipogenesis and gluconeogenesis [113][114][115][116].…”

Section: Ferulic Acidmentioning

confidence: 92%

The Use of Bioactive Compounds in Hyperglycemia- and Amyloid Fibrils-Induced Toxicity in Type 2 Diabetes and Alzheimer’s Disease

2022

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It has become increasingly apparent that defective insulin signaling may increase the risk for developing Alzheimer’s disease (AD), influence neurodegeneration through promotion of amyloid formation or by increasing inflammatory responses to intraneuronal β-amyloid. Recent work has demonstrated that hyperglycemia is linked to cognitive decline, with elevated levels of glucose causing oxidative stress in vulnerable tissues such as the brain. The ability of β-amyloid peptide to form β-sheet-rich aggregates and induce apoptosis has made amyloid fibrils a leading target for the development of novel pharmacotherapies used in managing and treatment of neuropathological conditions such as AD-related cognitive decline. Additionally, deposits of β-sheets folded amylin, a glucose homeostasis regulator, are also present in diabetic patients. Thus, therapeutic compounds capable of reducing intracellular protein aggregation in models of neurodegenerative disorders may prove useful in ameliorating type 2 diabetes mellitus symptoms. Furthermore, both diabetes and neurodegenerative conditions, such as AD, are characterized by chronic inflammatory responses accompanied by the presence of dysregulated inflammatory biomarkers. This review presents current evidence describing the role of various small bioactive molecules known to ameliorate amyloidosis and subsequent effects in prevention and development of diabetes and AD. It also highlights the potential efficacy of peptide–drug conjugates capable of targeting intracellular targets.

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Beneficial effects of ferulic acid alone and in combination with insulin in streptozotocin induced diabetic neuropathy in Sprague Dawley rats

Cited by 31 publications

References 59 publications

Association Between Serum Albumin Levels and Diabetic Peripheral Neuropathy Among Patients with Type 2 Diabetes: Effect Modification of Body Mass Index

Association Between Serum Albumin Levels and Diabetic Peripheral Neuropathy Among Patients with Type 2 Diabetes: Effect Modification of Body Mass Index

Ferulic acid alleviates sciatica by inhibiting neuroinflammation and promoting nerve repair via the TLR4/NF‐κB pathway

The Use of Bioactive Compounds in Hyperglycemia- and Amyloid Fibrils-Induced Toxicity in Type 2 Diabetes and Alzheimer’s Disease

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