Alcesefoliside protects against oxidative brain injury in rats

Simeonova, Rumyana; Vitcheva, Vessela; Kondeva-Burdina, Magdalena; G, Popov; Shkondrov, Aleksandar; Manov, Vasil; Krasteva, Ilina

doi:10.1016/j.bjp.2018.10.002

Cited by 12 publications

(7 citation statements)

References 26 publications

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“…In present study, treatment with walnut hull extract could significantly reduce the cortical architectural damage in cerebrum and preserve antioxidant system in rats challenged with ISO and these properties may be attributed to presence of polyphenolic components in hull extract of J. regia . Similar neuroprotective properties have been found in many other herbal ingredients against a wide variety of neurotoxic agents [ 56 , 57 ]. Even though, walnut hull is a byproduct but owing to its rich antioxidant makeup plus presence of excellent neuroprotective properties as shown in the current study, future research should be carried out to explore its neuroprotective potential against various nervous disorders.…”

Section: Discussionsupporting

confidence: 65%

Neuroprotective potential of hydroethanolic hull extract of Juglans regia L. on isoprenaline induced oxidative damage in brain of Wistar rats

Sharma¹,

Verma²,

Sood³

et al. 2021

Toxicology Reports

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Section: Discussionsupporting

confidence: 65%

Neuroprotective potential of hydroethanolic hull extract of Juglans regia L. on isoprenaline induced oxidative damage in brain of Wistar rats

Sharma¹,

Verma²,

Sood³

et al. 2021

Toxicology Reports

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“…The reduced glutathione (GSH) levels were measured according to the previously described method [ 57 , 58 ]. The principle of this assay was based on the reaction of DTNB with the sulfhydryl group of GSH that resulted in the development of a yellow color.…”

Section: Methodsmentioning

confidence: 99%

Suppression of TRPV1/TRPM8/P2Y Nociceptors by Withametelin via Downregulating MAPK Signaling in Mouse Model of Vincristine-Induced Neuropathic Pain

Khan

Shal

Khan

et al. 2021

IJMS

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Vincristine (VCR) is a widely used chemotherapy drug that induced peripheral painful neuropathy. Yet, it still lacks an ideal therapeutic strategy. The transient receptor potential (TRP) channels, purinergic receptor (P2Y), and mitogen-activated protein kinase (MAPK) signaling play a crucial role in the pathogenesis of neuropathic pain. Withametelin (WMT), a potential Phytosteroid isolated from datura innoxa, exhibits remarkable neuroprotective properties. The present investigation was designed to explore the effect of withametelin on VCR-induced neuropathic pain and its underlying molecular mechanism. Initially, the neuroprotective potential of WMT was confirmed against hydrogen peroxide (H2O2)-induced PC12 cells. To develop potential candidates for neuropathic pain treatment, a VCR-induced neuropathic pain model was established. Vincristine (75 μg/kg) was administered intraperitoneally (i.p.) for 10 consecutive days (day 1–10) for the induction of neuropathic pain. Gabapentin (GBP) (60 mg/kg, i.p.) and withametelin (0.1 and 1 mg/kg i.p.) treatments were given after the completion of VCR injection on the 11th day up to 21 days. The results revealed that WMT significantly reduced VCR-induced pain hypersensitivity, including mechanical allodynia, cold allodynia, and thermal hyperalgesia. It reversed the VCR-induced histopathological changes in the brain, spinal cord, and sciatic nerve. It inhibited VCR-induced changes in the biochemical composition of the myelin sheath of the sciatic nerve. It markedly downregulated the expression levels of TRPV1 (transient receptor potential vanilloid 1); TRPM8 (Transient receptor potential melastatin 8); and P2Y nociceptors and MAPKs signaling, including ERK (Extracellular Signal-Regulated Kinase), JNK (c-Jun N-terminal kinase), and p-38 in the spinal cord. It suppressed apoptosis by regulating Bax (Bcl2-associated X-protein), Bcl-2 (B-cell-lymphoma-2), and Caspase-3 expression. It considerably attenuated inflammatory cytokines, oxidative stress, and genotoxicity. This study suggests that WMT treatment suppressed vincristine-induced neuropathic pain by targeting the TRPV1/TRPM8/P2Y nociceptors and MAPK signaling.

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“…Tissue homogenates (10% w/v) were prepared in cold 0.1 M phosphate buffer solution (pH 7.4) and used to determine MDA formation 53 . Cell debris was removed by centrifugation (10000× g at 4°C for 20 min) and the supernatant was assayed to determine nitrite levels 54 and enzyme antioxidants, viz. superoxide dismutase 55 , CAT 56 , and reduced GSH 57 .…”

Section: Methodsmentioning

confidence: 99%

Antidiabetic Activity of Caulerpa racemosa: Role of Proinflammatory Mediators, Oxidative Stress, and Other Biomarkers

Mandlik

Naik²,

Zine

et al. 2022

Planta Medica International Open

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A marine alga, Caulerpa racemose (seaweed), exhibits few biological activities, such as antinociceptive/anti-inflammatory, antitumor, and growth regulator. This study aimed to determine the antidiabetic activity of this seaweed. High-performance thin-layer chromatography of C. racemosa ethanolic extract was performed to identify its active constituents. Antidiabetic activity of C. racemosa ethanolic extract (100 and 200 mg/kg) was evaluated using various biochemical paradigms against glipizide (5 mg/kg) in a streptozotocin-induced diabetes rat model. High-performance thin-layer chromatography revealed β-sitosterol as an active constituent and also indicated the presence of saponins and alkaloids. Treatment with C. racemosa ethanolic extract significantly reduced blood glucose levels in diabetic rats, and the degree of glucose reduction was comparable to that attained by glipizide treatment. The C. racemosa ethanolic extract treatment restored the impaired glycosylated hemoglobin level, liver glycogen level, glucose uptake by hemidiaphragm, and glucose transport by hepatic cells. Pretreatment with C. racemosa ethanolic extract also restored lipid abnormalities, elevated liver enzymes, elevated inflammatory markers, and depleted endogenous antioxidants. A superior effect was shown by C. racemosa ethanolic extract (200 mg/kg) over glipizide (5 mg/kg). Moreover, the restoration of the histoarchitecture of the pancreas by C. racemosa ethanolic extract (200 mg/kg) was comparable to that of the glipizide (5 mg/kg) treatment group. The present experimental findings demonstrate significant antidiabetic activity of C. racemosa ethanolic extract in diabetic rats using various biochemical paradigms. Further, C. racemosa ethanolic extract seems to be safe and does not affect vital organs adversely.

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Alcesefoliside protects against oxidative brain injury in rats

Cited by 12 publications

References 26 publications

Neuroprotective potential of hydroethanolic hull extract of Juglans regia L. on isoprenaline induced oxidative damage in brain of Wistar rats

Neuroprotective potential of hydroethanolic hull extract of Juglans regia L. on isoprenaline induced oxidative damage in brain of Wistar rats

Suppression of TRPV1/TRPM8/P2Y Nociceptors by Withametelin via Downregulating MAPK Signaling in Mouse Model of Vincristine-Induced Neuropathic Pain

Antidiabetic Activity of Caulerpa racemosa: Role of Proinflammatory Mediators, Oxidative Stress, and Other Biomarkers

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