Abstract
Cigarette smoking (CS) is a major health hazard that exerts diverse physiologic and biochemical effects mediated by the components present and generated during smoking. Recent experimental studies have shown predisposition to several biological consequences from both active and passive cigarette smoke exposure. In particular, passive smoking is linked to a number of adverse health effects which are equally harmful as active smoking. A pragmatic approach should be considered for designing a pharmacological intervention to combat the adverse effects of passive smoking. This review describes the results from a controlled experimental condition, testing the effect of bacoside A (BA) on the causal role of passive/secondhand smoke exposure that caused pathological and neurological changes in rat brain. Chronic exposure to cigarette smoke induced significant changes in rat brain histologically and at the neurotransmitter level, lipid peroxidation states, mitochondrial functions, membrane alterations, and apoptotic damage in rat brain. Bacoside A is a neuroactive agent isolated from Bacopa monnieri. As a neuroactive agent, BA was effective in combating these changes. Future research should examine the effects of BA at molecular level and assess its functional effects on neurobiological and behavioral processes associated with passive smoke.
Highlights
Cigarette smoking is an intractable and preventable public health problem
Cigarette smoking is associated with diverse structural changes in brain, probably as a consequence of toxicity or as an adaptive response, causing a reduction in integrity of cerebral white matter microstructure [82] and gray matter volumes [83, 84] and these changes appear correlated with the magnitude of cigarette exposure
Histological changes were prevalent in brain of rats exposed to cigarette smoke that were inflammatory and edematous in the cerebrum (Figure 1)
Summary
Cigarette smoking is an intractable and preventable public health problem. It is an important risk factor involved in the pathogenic pathways of a variety of disorders. Etiological evidences support the involvement of neurotransmitter systems, oxidative and nitrogen stress, mitochondrial dysfunction, and neurogenetic and epigenetic changes in secondhand/passive smoking induced brain changes and the associated pathways have been extensively reviewed [8,9,10,11]. This review critically examines and summarizes the study made on the neuroprotective role of BA in rats exposed to passive cigarette smoke and its sequelae with focus on the neurotransmitter systems, oxidative and lipid peroxidative, mitochondrial dysfunction, and apoptotic changes in rat brain. These results can be integrated with other theories in holistically combating passive smoking induced neurological changes
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