Stroke is recognized as one of the most dangerous killer diseases in Thailand and other countries worldwide. The development of a novel strategy for treating stroke patients is therefore urgently required. The present study investigated the effect of laser acupuncture at the Baihui point on cognitive and functional recovery, neuronal loss, antioxidant enzyme activities, and interleukin-6 (IL-6) activity in the hippocampus in an animal model of focal ischemic stroke. Male Wistar rats were randomly divided into 4 groups: sham operation; permanent occlusion of the right middle cerebral artery (Rt.MCAO); Rt.MCAO with sham laser acupuncture; and Rt.MCAO with Baihui point laser acupuncture. Laser acupuncture at the Baihui point and sham acupuncture at a nonacupoint were performed once daily (10 min at each point) for 14 days after Rt.MCAO. Half of the rats in each group were examined to determine neuron density by Cresyl violet staining, while the other half were examined by biochemical assays to measure glutathione peroxidase (GSH-Px) in the hippocampus, superoxide dismutase (SOD) in mitochondria and interleukin-6 (IL-6) activity in the hippocampus. Laser acupuncture treatment was found to significantly enhance memory and neuron density in CA1 and CA3. Improved neurological score, improved GSH-Px and SOD activities, and decreased density ratio of IL-6 toβ-actin were also observed in the hippocampus. In conclusion, Baihui point laser acupuncture alleviates cognitive impairment and motor deficits via antioxidant and anti-inflammatory effects in focal ischemic rats. Further study is warranted to investigate other possible mechanisms of action.

The burden of stroke is high and is continually increasing due to a dramatic growth in the world's elderly population. Novel therapeutic strategies are therefore required. The present study sought to determine the effect of laser acupuncture at GV20 on brain damage, oxidative-status markers in the cerebral cortex, and superoxide dismutase in the mitochondria of an animal model of focal ischemic stroke. Wistar rats, weighing 300-350 g, were divided into the following four groups: (1) control; (2) permanent occlusion of the right middle cerebral artery (Rt.MCAO) alone; (3) Rt.MCAO plus sham laser acupuncture; and (4) Rt.MCAO plus laser-acupuncture groups. Sham laser acupuncture or laser acupuncture was performed once daily at the GV20 (Baihui) acupoint for 14 days following Rt.MCAO. Half of the rats in each group were examined by 2,3,5-triphenyltetrazolium chloride staining to determine the brain infarct volume, while the other half were examined by biochemical assays to determine the malondialdehyde level, and the glutathione peroxidase, catalase, and superoxide-dismutase activities in the brain-cortex mitochondria. The results showed that laser acupuncture at GV20 significantly decreased the brain infarct volume and malondialdehyde level, and increased the catalase, glutathione peroxidase, and superoxide-dismutase activities in cerebral ischemic rats. In conclusion, laser acupuncture at GV20 decreases the brain infarct volume in cerebral ischemic rats, at least in part due to decreased oxidative stress. Further study is warranted to investigate other possible underlying mechanisms.

The neuroprotectant and memory enhancer supplement for menopause is required due to the side effects of hormone replacement therapy. Since purple waxy corn cob and pandan leaves exert antioxidant and acetylcholinesterase inhibition (AChEI) effects, we hypothesized that the combined extract of both plants (PCP) might provide synergistic effect leading to the improved brain damage and memory impairment in experimental menopause. To test this hypothesis, female Wistar rats were ovariectomized bilaterally and orally given various doses of the functional drink at doses of 20, 40, and 80 mg/kg for 28 days. The animals were assessed nonspatial memory using object recognition test every 7 days throughout the study period. At the end of study, they were assessed with oxidative stress status, AChEI, neuron density, and ERK1/2 signal in the prefrontal cortex (PFC). Interestingly, all doses of PCP increased object recognition memory and neuron density but decreased oxidative stress status in PFC. Low dose of PCP also decreased AChE activity while medium dose of PCP increased phosphorylation of ERK1/2 in PFC. Therefore, the improved oxidative stress status and cholinergic function together with signal transduction via ERK in PFC might be responsible for the neuroprotective and memory‐enhancing effects of PCP.

Focal ischemia occurs when an embolus or thrombus occludes an artery, causing the rapid obstruction of cerebral blood flow. Although stroke represents a main cause of disability and mortality in developing countries, therapeutic approaches available for this condition remain very limited. The aim of the present study was to examine the effects of the phytochemical, 6‑gingerol, on the brain infarct volume, neuronal loss and on the oxidative stress parameters, cyclooxygenase‑2 (COX‑2) and interleukin (IL)‑6, in an animal model of focal ischemic stroke. Male Wistar rats, weighing 250‑300 g, were divided into the following six groups: i) The control; ii) right middle cerebral artery occlusion (Rt.MCAO) + vehicle; iii) Rt.MCAO + piracetam; iv) Rt.MCAO + 6‑gingerol (6‑Gin) at 5 mg/kg body weight (BW); v) Rt.MCAO + 6‑Gin at 10 mg/kg BW; and vi) the Rt.MCAO + 6‑Gin at 20 mg/kg BW group. The rats in each group received the vehicle or piracetam or 6‑gingerol intraperitoneally for 7 days following Rt.MCAO. The brain infarct volume, neuronal loss and alterations in antioxidant and anti‑inflammatory levels were assessed in the cortex and hippocampus. The results revealed that the brain infarct volume, malondialdehyde level and the density ratio of COX‑2 and IL‑6 to β‑actin were significantly decreased following treatment with 6‑gingerol. In addition, neuronal density and superoxide dismutase activity in the cortex and hippocampus were increased. On the whole, the findings of the present study suggest that 6‑gingerol exerts antioxidant and anti‑inflammatory effects in vivo, which effectively ameliorate the brain damage induced by focal cerebral ischemic stroke.

The rising incidence of ischemic stroke poses significant health and healthcare burdens. Given the limitations of current therapeutic options, there is increasing interest in exploring the potential of galangin, a natural flavonoid compound, as a treatment for ischemic stroke. This study aimed to evaluate the neuroprotective effects and underlying mechanisms of galangin in mitigating oxidative stress, inflammation, and apoptosis in a rat model of permanent cerebral ischemia. Sixty male Wistar rats were divided into six groups: control; right middle cerebral artery occlusion (Rt.MCAO) with vehicle; Rt.MCAO with piracetam, a synthetic compound known as a cognitive enhancer; and Rt.MCAO with galangin administered at doses of 25, 50, and 100 mg/kg body weight. Neurological deficit scores, brain edema, neuronal density, and microglial morphology were assessed along with the activity of myeloperoxidase (MPO), a marker of inflammation, and superoxide dismutase (SOD). Additionally, the expression of key markers for inflammation and apoptosis, cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), Bcl-2-associated X protein (Bax), B-cell lymphoma-extra large (Bcl-XL), and caspase-3, was analyzed to elucidate potential mechanisms. The results demonstrated that galangin treatment significantly improved neurological deficit scores, reduced brain edema, enhanced neuronal density, attenuated microglial activation, decreased MPO activity, and increased SOD activity in both the cortex and hippocampus, highlighting its neuroprotective potential. These effects were linked to the modulation of inflammatory and apoptotic pathways. Specifically, galangin significantly reduced the expression of IL-6, COX-2, Bax, and caspase-3 while increasing the levels of the anti-apoptotic protein Bcl-XL. In conclusion, galangin demonstrates significant promise as a neuroprotective agent for ischemic stroke by suppressing inflammation and apoptosis, thereby improving neurological outcomes. However, clinical trials are required to validate these preclinical findings and confirm galangin’s therapeutic efficacy in humans.