Nicotinamide reduces infarction up to two hours after the onset of permanent focal cerebral ischemia in Wistar rats
Section snippets
Acknowledgements
The authors thank Dr. Adelbert Ames III and Dr. Eng H. Lo for constructive comments on the manuscript. K.I.M. is an American Heart Association Minority Scientist Development Awardee; C.S.O. is supported by NIH grant #NS01732, and M.F.B. is supported by NIH grants #NS32365 and #NS31579.
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Pharmacokinetics of the SABRE agent 4,6-d <inf>2</inf> -nicotinamide and also nicotinamide in rats following oral and intravenous administration
2019, European Journal of Pharmaceutical SciencesCitation Excerpt :The pharmacokinetics of NA are known to be dependent on dose, species, sex and route of administration. Safe doses in rats have previously been characterized: 750 mg/kg for subcutaneous injection and 1000 mg/kg for IP injection (Ayouba et al., 1999) Furthermore, intravenous (IV) doses of 750 mg/kg in rat models of stroke (Sakakibara et al., 2000) have been used. An in vitro cytotoxicity study demonstrated that it is possible to create a biocompatible SABRE bolus of d2-NA and that deuteration of NA does not increase the toxicity compared to the NA (Manoharan et al., 2018).
Effects of nicotinamide on spatial memory and inflammation after juvenile traumatic brain injury
2019, Behavioural Brain ResearchTherapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence
2018, Cell MetabolismNicotinamide mononucleotide inhibits post-ischemic NAD<sup>+</sup> degradation and dramatically ameliorates brain damage following global cerebral ischemia
2016, Neurobiology of DiseaseCitation Excerpt :However, since PAR is consumed by poly-ADP-ribose glycohydrolase (PARG) (Davidovic et al., 2001), the above statement is valid under the assumption that there is no effect of NMN on PAR degradation by PARG. Administration of Nam also protects against excitotoxic and ischemic cell death (Ayoub et al., 1999; Yang et al., 2002a, Liu et al., 2009). It was reported that Nam exerts a number of pharmacological effects including prevention of ATP depletion (Yang et al., 2002b), inhibition of PARP1 (Klaidman et al., 1996; Yang et al., 2002b, Liu et al., 2009), lipid peroxidation (Liu et al., 2009; Klaidman et al., 2001), anti-inflammatory activity (Ungerstedt et al., 2003), and prevention of apoptosis (Klaidman et al., 1996, 2001).