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Micronutrients in Prevention and Improvement of the Standard Therapy in Diabetes
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
Diabetes can lead to thiamine deficiency. Treatment of streptozotocin-induced diabetic mice with benfotiamine, a lipophilic derivative of thiamine, reduced cerebral oxidative stress without affecting the levels of advanced glycation end-product (AGE), protein carbonyl, tissue factor, and TNF-alpha.189 These results suggest that the primary action of benfotiamine is mediated via antioxidation.
Alcohol, Ageing and Cognitive FunctionA nutritional perspective
Published in Jenny Svanberg, Adrienne Withall, Brian Draper, Stephen Bowden, Alcohol and the Adult Brain, 2014
Thiamine is a water-soluble vitamin occurring in free or phosphorylated forms in most plant and animal tissues. Lipid-soluble precursors of thiamine have a higher bioavailability than the basic thiamine molecule. Benfotiamine (s-benzoylthiamine) has been found to prevent the progression of diabetes, but does not alter brain levels of thiamine. More effective lipid-soluble compounds, such as allithiamine and synthetic sulbutiamine and fursultiamine, do increase levels of brain thiamine (Volvert et al., 2008).
Thiamine alleviates cognitive impairment and epileptogenesis by relieving brain inflammation in PTZ-induced kindling rat model
Published in Neurological Research, 2022
Sebahattin Karabulut, Ahmet Kemal Filiz, Recep Akkaya
It suggests that inflammation and seizures contribute to neuropsychiatric comorbidities of epilepsy [42]. Moreover, cognitive impairments such as spatial memory deficit frequently manifest in patients with epilepsy [43]. Consistent with our results, it has been shown in previous studies that PTZ-induced epileptogenesis causes learning and memory impairments [44,45]. Chemical kindling induced by PTZ leads to structural pathological changes, oxidative stress, and neuroinflammation in the hippocampus, which is the essential structure of the brain in learning and memory [46,47]. Our results showed that thiamine pretreatment alleviated learning deficits caused by PTZ-kindling. A recent experimental study showed that oral benfotiamine supplementation increased thiamine diphosphate concentrations in the hippocampus and entorhinal cortex, and it improved the STZ-related cognitive deficit in rats [48]. Evidence indicates that thiamine is a neuroinflammation modulator known for removing reactive oxidative species [12,49]. Also, previous studies reported that benfotiamine can exert antiinflammatory effects [50,51]. Considering the constantly increasing oxidative stress and inflammation in the epileptic hippocampus, it is plausible that the neuroprotective effect of thiamine is likely a result of its potent anti-inflammatory effect.
Pristimerin inhibits neuronal inflammation and protects cognitive function in mice with sepsis-induced brain injuries by regulating PI3K/Akt signalling
Published in Pharmaceutical Biology, 2021
Weimin Xue, Yaqiang Li, Mei Zhang
LPS induces both sepsis and neuronal injury caused by various cytokines. Benfotiamine, a derivative of thiamine monophosphate, reportedly protects BV-2 microglia from the effects of LPS by blocking PI3K/Akt signalling, thus reducing NO production; iNOS, Cox-2 and Hsp70 expression; and TNF-α and IL-6 synthesis. Phosphoinositide 3-kinases (PI3Ks) regulate several key steps in the inflammatory response to external insults (Redza-Dutordoir and Averill-Bates 2016). PI3Ks transduce signals from growth factors, cytokines, hormones and LPS to intracellular messages, thereby generating phospholipids. These phospholipids activate the serine/threonine kinase Akt and other downstream effector pathways. The eight PI3Ks of mammalian cells are divided into three families (Liu et al. 2014) that differ in terms of regulation and the preferred lipid substrate. PI3K lipid kinases are involved in many cellular functions, including signal transduction and intracellular vesicular trafficking; PI3K pathway dysregulation is a feature of several pathological conditions, including neurological diseases. PI3K/Akt pathway inhibition in LPS-activated microglia reduced the levels of proinflammatory factors (Zhou et al. 2020). However, another study found that PI3K/Akt activation attenuated brain damage by upregulating the anti-oxidative response and inhibiting inflammation and apoptosis. In the present study, PI3K/Akt signalling was ameliorated by pristimerin in brain-injured mice. Histopathology findings also suggested that pristimerin ameliorated injury.
Pharmacotherapeutic options for co-morbid depression and alcohol dependence
Published in Expert Opinion on Pharmacotherapy, 2019
Thomas Hillemacher, Helge Frieling
Chronic alcoholism is frequently associated with significant nutritional and vitamin deficiencies, including vitamin B1 (thiamine) deficiency that is associated with depression and other psychiatric disorders [102]. Approximately 30–80% of inpatients admitted for alcohol treatment are thiamine deficient [102]. Benfotiamine, a synthetic S-acyl thiamine derivative, significantly ameliorates mitochondrial dysfunction and attenuates oxidative damage and inflammation [103]. Manzardo et al. evaluated the efficacy of the benfotiamine in a 6-month randomized, double-blind, placebo-controlled clinical pilot trial [102]. They randomized 85 male patients with current DSM-IV diagnoses of alcohol dependence with or without depressive symptoms on benfotiamine (600 mg/d) or placebo. The results suggested that thiamine deficiency contributes significantly to psychiatric distress in severe AUD supporting the possible benefit of thiamine supplementation for the alleviation of depressive symptomatology in patients with AUD. This can be considered an adjuvant therapy in alcohol rehabilitation [102].