Elucidation of ameliorative effect of Co-enzyme Q10 in streptozotocin-induced diabetic neuropathic perturbation by modulation of electrophysiological, biochemical and behavioral markers

Visnagri, Asjad; Kandhare, Amit D.; Kumar, V. Shiva; Rajmane, Anuchandra Ramchandra; Adil, Malik M; Ghosh, Pranab; Ghule, Arvindkumar E.; Bodhankar, Subhash L.

doi:10.1016/j.biomag.2012.10.006

Cited by 69 publications

(35 citation statements)

References 93 publications

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“…[41][42][43][44] Several lines of studies reported that GM-induced GSH level depletion might be due to excess generation of free radicals or increased consumption in the protection of -SH group-containing proteins and decreased SOD antioxidant enzymes associated with overproduction of superoxide anions and hydrogen peroxide. 18,[45][46][47] In consistent with the previous finding, our results showed that GM administration increased MDA level as an end product of lipid peroxidation while decreased GSH and SOD levels in renal tissue. 48 The present finding indicated that berberine treatment restore the MDA, GSH and SOD levels in renal tissue of GM-induced toxicity groups via its free radical scavenging and/or increasing antioxidant property.…”

Section: Discussionsupporting

confidence: 92%

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

et al. 2016

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Background: Gentamicin (GM) is the commonly used antibiotics against Gram-negative infection, but the nephrotoxic potential of drug limit its clinical interest. The aim of this study was to investigate the protective effect of berberine (BER) against GM-induced nephrotoxicity and possible underlying mechanisms. Material and methods: The rats were divided into various group, namely normal, GM-control, GM þ BER (10, 20, and 40 mg/kg). Nephrotoxicity was induced by intraperitoneal administration of GM (120 mg/kg) for 7 consecutive days. BER (10, 20, and 40 mg/kg; p.o.) was also administered for the 7 days. Various biochemical, molecular, and histological parameters were assessed in serum and kidney. Results: GM-administration significantly increased (p < 0.001) the serum creatinine and blood urea nitrogen (BUN) as well as renal malonaldehyde (MDA), nitric oxide (NO) along with Kidney Injury Molecule-1 (KIM-1), Neutrophil gelatinase-associated lipocalin (NGAL), and nuclear factor-kappa B (NF-KB) renal mRNA expressions. In addition, GM also significantly decreased (p < 0.001) the renal superoxide dismutase (SOD), reduced glutathione (GSH), B-cell lymphoma 2 (Bcl-2) mRNA expression, and mitochondrial enzymes (NADH dehydrogenase and cytochrome c oxidase) activities. Rats treated with BER (20 and 40 mg/kg; p.o.) significantly and dose-dependently (p < 0.05 and p < 0.01) restore the altered levels of antioxidant, inflammatory, apoptosis, AKI markers as well as depleted mitochondrial enzymes. Histopathological abbreviations were also ameliorated by BER administration. Conclusion: Berberine exerts renoprotective effects through its anti-oxidant, anti-inflammatory, and anti-apoptotic properties.

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Section: Discussionsupporting

confidence: 92%

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

et al. 2016

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“…45 Any form of interruption in the angiogenesis process may further progress to variable diseases such as retinopathy, neuropathy, prolonged lung disorders, and arthritis. 46 Non-biologically differentiated microangiopathy during diabetes may lead to depletions of cellular growth requirements that progress to retarded wound healing. 47 VEGF may be among the various effective single growth treatment targets.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin enhances angiogenesis via modulating expression of growth and inflammatory factor in diabetic foot ulcer in rats

Wang

et al. 2018

Eur J Inflamm

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One of the most devastating consequences of diabetes mellitus is a chronic condition, diabetic foot ulcer. Numerous investigations are being targeted to explore newer compounds for treatment of diabetic foot ulcer wounds in diabetic patients. Hesperidin (HSP), an isoflavone glycoside has been established to exhibit antidiabetic and antioxidant potential. In the current investigation, diabetes was induced in rats by administration by streptozotocin (STZ) intraperitoneally (50 mg/kg). Wound-healing capacity was estimated in hind paw of rats by artificially initiating wound injury on the paw dorsal surface. The injured animals were administered with incremental doses of HSP suspension orally (10,20,40, 60, and 80 mg/kg) and insulin subcutaneously (10 IU/kg). Parameters such as wound area were estimated every 2 days, and at the end of 20 days of study, biochemical estimations in serum and histopathological observations of the wound were made. HSP (60 and 80 mg/kg) revealed statistically significant (P < 0.05) improvement in wound dimension, glucose and insulin concentration, and glycated hemoglobin (HbA1C). Administration of HSP indicated significant (P < 0.05) modulation of mRNA associated with expression of vascular endothelial growth factor (VEGF), whereas the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels were lowered compared to the control group of animals. Real-time quantitative polymerase chain reaction (RT-qPCR) indicated expression of vascular endothelial growth factor receptors 1 and 2 (VEGFR1 and VEGFR2) compared to glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Histological observations indicated higher expression of VEGF in the groups receiving HSP, indicative of angiogenesis stimulation in the diabetic wound. The results advocate angiogenesis activity of HSP was enhanced owing to reduction in hyperglycemia and oxidative stress-induced damage, reduced expression of inflammatory mediators, and enhanced expression of growthrelated factors, thereby promoting healing of diabetic foot ulcer.

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“…MDA indicates high oxidative stress because of the destruction of lipid membrane, particularly fatty acids of unsaturated bonds Visnagri et al, 2012). Inhibition of lipid peroxidation by flavonoids is supposed to increase the viability of collagen fibrils by activating DNA synthesis and preventing cell damage (Shetty et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Wound healing potential of naringin ointment formulation via regulating the expression of inflammatory, apoptotic and growth mediators in experimental rats

Kandhare

Alam

Patil

et al. 2015

Pharmaceutical Biology

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Context: Wound healing is a consequence of a complex process involving inflammatory, proliferative, and remodeling phases. Naringin, a flavanone glycoside, is associated with modulation of various oxido-inflammatory and growth factors. Aim: The aim of this study is to evaluate the wound-healing activity of naringin ointment formulation (NOF) on experimental wound models. Materials and methods: A soft paraffin-based cream containing 1, 2, and 4% (w/w) naringin was formulated and evaluated for physicochemical characters. Excision wounds and incisions wounds were used to study the topical effect of NOF for 20 d (once a day) on various biochemical, molecular, and histological parameters. Results: NOF (2 and 4%, w/w) treatment showed a significant decrease (p50.05) in wound area and epithelization period whereas the rate of wound contraction increased significantly (p50.05). The altered levels of oxido-nitrosative stress (SOD, GSH, MDA, MPO, and NO) were significantly (p50.05) restored by NOF. Treatment produced a significant increase (p50.05) in tensile strength, hydroxyproline content, and protein content. TNF-a, IL-1b, IL-6, IL-8, NF-jB, smad-7, and Bax mRNA expression were significantly down-regulated (p50.05) by NOF, whereas polymerase gamma (pol-g), smad-3, VEGF and TGF-b, and collagen-1 mRNA expressions were significantly up-regulated (p50.05) by NOF. Histological alterations in wound skin were also restored by NOF. Conclusion: NOF exerts wound healing potential via down-regulated expression of inflammatory (NF-jB, TNF-a, and ILs), apoptotic (pol-g and Bax), and up-regulated growth factor (VEGF and TGF-b) expression, thus modulating collagen-1 expression to induce angiogenesis leading to wound healing.

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Elucidation of ameliorative effect of Co-enzyme Q10 in streptozotocin-induced diabetic neuropathic perturbation by modulation of electrophysiological, biochemical and behavioral markers

Cited by 69 publications

References 93 publications

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

Ameliorative effect of berberine against gentamicin-induced nephrotoxicity in rats via attenuation of oxidative stress, inflammation, apoptosis and mitochondrial dysfunction

Hesperidin enhances angiogenesis via modulating expression of growth and inflammatory factor in diabetic foot ulcer in rats

Wound healing potential of naringin ointment formulation via regulating the expression of inflammatory, apoptotic and growth mediators in experimental rats

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