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    Cucurbita pepo seeds improve peripheral neuropathy in diabetic rats by modulating the inflammation and oxidative stress in rats
    (Springer Science and Business Media Deutschland GmbH, 2023-07-03T00:00:00) Kaur, Navpreet; Kishore, Lalit; Farooq, Shah Asma; Kajal, Anu; Singh, Randhir; Agrawal, Rohini; Mannan, Ashi; Singh, Thakur Gurjeet
    Background: Cucurbita pepo (C. pepo) is cultivated and used traditionally as vegetable as well as medicine in different parts of the world. The aim of current study was to investigate the potential of C. pepo in attenuation of diabetic neuropathy via using streptozotocin (STZ)-induced diabetes model in male wistar rats. Materials and Methods: Diabetic neuropathy was induced by administration of STZ; 65�mg/kg, i.p. and Nicotinamide (NAD; 230�mg/kg i.p.) and assessed by measuring thermal hyperalgesia, mechanical hyperalgesia and motor nerve conduction velocity (MNCV) in experimental animals. Treatment with different doses of (100, 200 and 400�mg/kg, p.o.) petroleum ether extract of C. pepo (CPE) and hydroethanolic extract of C. pepo (CHE) was started from the 60th day of STZ/NAD administration and continued upto 90th day. Results: CPE and CHE significantly attenuated the behavioural changes including hyperalgesia, allodynia and MNCV linked to diabetic neuropathy. Moreover, the oxidative stress and level of TNF-?, TGF-? and IL-1? was found to be significantly attenuated in experimental animals. Conclusion: Thus C. pepo might ameliorate the progression of diabetic neuropathy via modulation of chronic hyperglycemia and therefore and have therapeutic potential for treatment of diabetic neuropathic pain. � 2023, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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    Quercetin Exhibits ?7nAChR/Nrf2/HO-1-Mediated Neuroprotection Against STZ-Induced Mitochondrial Toxicity and Cognitive Impairments in Experimental Rodents
    (Springer, 2021-09-23T00:00:00) Singh, Niraj Kumar; Garabadu, Debapriya
    The objective of the present study was to investigate the ?7nAChR-mediated Nrf2-dependant protective activity against streptozotocin (STZ)-induced brain mitochondrial toxicity in Alzheimer�s disease (AD)-like rats. STZ (3�mg/kg) was injected through an intracerebroventricular route to induce AD-like dementia. Repeated Quercetin (50�mg/kg, i.p.) administration attenuated cognitive impairments in the STZ-challenged animals during Morris water-maze and Y-maze tests. Quercetin significantly mitigated the STZ-induced increase in cholinergic dysfunction, such as the increase in acetylcholinesterase activity, decrease in acetylcholine level, and activity of choline acetyltransferase, and increase in amyloid-beta aggregation and mitochondrial toxicity in respect of mitochondrial bioenergetics, integrity, and oxidative stress in memory-challenged rat hippocampus, prefrontal cortex and, amygdala. Further, Quercetin significantly attenuated STZ-induced reduction in the ?7nAChRs and HO-1 expression levels in the selected rat brain regions. On the contrary, trigonelline (10�mg/kg, i.p.) and methyllycaconitine (2�mg/kg; i.p.) abolished the neuroprotective effects of Quercetin against STZ-induced behavioral, molecular, and biochemical alterations in the AD-like animals. Hence, Quercetin exhibits ?7nAChR/Nrf2/HO-1-mediated neuroprotection against STZ-challenged AD-like animals. Thus, Quercetin could be considered as a potential therapeutic option in the management of AD. Graphical Abstract: [Figure not available: see fulltext.] � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.