Srikiatkhachorn, Anan

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Preferred name
Srikiatkhachorn, Anan
Alternative Name
Srikiatkhachorn, Anon
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Email
anan.sr@kmitl.ac.th

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    Long-Term Paracetamol Treatment Impairs Cognitive Function and Brain-Derived Neurotrophic Factor in Adult Rat Brain
    (2023-01-01)
    Lalert, Laddawan
    ;
    Tantarungsee, Nutnicha
    ;
    Chotipinit, Tipthanan
    ;
    Ji-au, Wilawan
    ;
    Srikiatkhachorn, Anan
    Paracetamol (acetaminophen, APAP) is known as a safe pain reliever; however, its negative effects on the central nervous system have gradually been reported. We examined alterations in learning and memory, and brain-derived neurotrophic factor (BDNF) expression in the frontal cortex and hippocampus at different durations of APAP treatment in rats. Novel object recognition (NOR) and Morris water maze (MWM) paradigms were used to assess learning and memory in rats fed with 200 mg/kg APAP at single-dose, 15-day or 30-day treatments. BDNF expression was evaluated through immunohistochemistry and Western blotting. The single-dose APAP treatment did not alter the NOR performance. However, deficits in the NOR and MWM capacities were detected in the rats with longer durations of APAP treatment. An analysis of BDNF expression revealed no significant change in BDNF expression in the single-dose APAP treatment, while rats given APAP for extended periods as treatment showed a significant decrement in this protein in the frontal cortex and hippocampus. Short-term APAP treatment has no effect on learning and memory, or BDNF expression; however, long-term APAP exposure causes cognitive impairment. The diminishment of the BDNF level in the frontal cortex and hippocampus due to the long period of treatment with APAP may at least in part be involved in altered learning and memory in rats.
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    Alterations in Synaptic Plasticity and Oxidative Stress Following Long-Term Paracetamol Treatment in Rat Brain
    (2020-02-01)
    Lalert, Laddawan
    ;
    Ji-au, Wilawan
    ;
    Srikam, Sirinapa
    ;
    Chotipinit, Tipthanan
    ;
    Sanguanrungsirikul, Sompol
    Several studies have recently revealed that cognitive function can be affected by paracetamol (APAP) treatment. However, the exact impact of this drug treatment on learning and memory has not been clarified. This study aimed to investigate the effect of APAP treatment on the alteration of synapses and oxidative stress in the rat frontal cortex and hippocampus. APAP at a dose of 200 mg/kg bw was fed to adult male Wistar rats through either acute (n = 10), 15-day (n = 10), or 30-day (n = 10) treatment regimens. The synaptic ultrastructure and proteins, synaptophysin (SYP) and postsynaptic density-95 (PSD-95), were monitored. The amount of protein carbonyl oxidation (PCO) and glutathione (GSH) levels were examined. Our results demonstrated that acute treatment with APAP had no effect on synapses and oxidative stress. However, the synapses obtained from rats with 15-day APAP treatment showed a marked shortening of active zones and widening of the synaptic cleft. Decrement of SYP and PSD-95 proteins were demonstrated in these rats as well. With 30-day APAP treatment, the alteration of the synaptic ultrastructure and proteins was more evident. Moreover, the depletion of GSH and the elevation of PCO levels were demonstrated in the rats treated with APAP for 30 days. These results suggest that long-term APAP treatment can induce synaptic degeneration in the hippocampus and frontal cortex. The increase in oxidative stress in these brain areas may be due to the deleterious effect of this drug.