Summary: Hearing loss is frequent in intensive care patients and can be due to several causes. However, sepsis has not been examined as a possible cause. The aim of this study is to assess the influence of experimental sepsis on hearing thresholds and to evaluate pathological changes in the cochlea. The cecal ligation puncture technique was used to induce sepsis in 18 mice. Results were compared with those from 13 sham-operated and 13 untreated control mice. The hearing thresholds of the animals were evaluated with auditory evoked brainstem responses prior to the induction of sepsis and again at the peak of the disease. Immediately after the second measurement, the mice were sacrificed and the inner ears harvested and prepared for further evaluation. The cochleae were examined with light microscopy, electron microscopy and immunohistochemistry for Bax, cleaved caspase-3 and Bcl-2. The mice with sepsis showed a significant hearing loss but not the control groups. Induction of apoptosis could be shown in the supporting cells of the organ of Corti. Furthermore, excitotoxicity could be shown at the basal pole of the inner hair cells. In this murine model, sepsis leads to significant hearing impairment. The physiological alteration could be linked to apoptosis in the supporting cells of the organ of Corti and to a disturbance of the synapses of the inner hair cells.

Oxidative stress plays a role in the delay of peripheral nerve regeneration after injury. The accumulation of free radicals results in nerve tissue damage and dorsal root ganglion (DRG) neuronal death. Pinostrobin (PB) is one of the bioflavonoids from Boesenbergia rotunda and has been reported to possess antioxidant capacity and numerous pharmacological activities. Therefore, this study aimed to investigate the effects of PB on peripheral nerve regeneration after injury. Male Wistar rats were randomly divided into 5 groups including control, sham, sciatic nerve crush injury (SNC), SNC + 20 mg/kg PB, and SNC + 40 mg/kg PB. Nerve functional recovery was observed every 7 days. At the end of the study, the sciatic nerve and the DRG were collected for histological and biochemical analyses. PB treatment at doses of 20 and 40 mg/kg reduced oxidative stress by up-regulating endogenous glutathione. The reduced oxidative stress in PB-treated rats resulted in increased axon diameters, greater number of DRG neurons, and p-ERK1/2 expression in addition to faster functional recovery within 4 weeks compared to untreated SNC rats. The results indicated that PB diminished the oxidative stress-induced nerve injury. These effects should be considered in the treatment of peripheral nerve injury.

Background: One of the most common neurodegenerative diseases is Parkinson’s disease (PD); PD is characterized by a reduction of neurons containing dopamine in the substantia nigra (SN), which leads to a lack of dopamine (DA) in nigrostriatal pathways, resulting in motor function disorders. Oxidative stress is considered as one of the etiologies involved in dopaminergic neuronal loss. Thus, we aimed to investigate the neuroprotective effects of pinostrobin (PB), a bioflavonoid extracted from Boesenbergia rotunda with antioxidative activity in PD. Methods: Rats were treated with 40 mg/kg of PB for seven consecutive days before and after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. After completing the experiment, the brains including SN and striatum were used for histological studies and biochemical assays. Results: PB treatment demonstrated a reduction of free radicals in the SN as indicated by significantly decreased MDA levels, whereas the antioxidative enzymes (SOD and GSH) were significantly increased. Furthermore, PB treatment significantly increased glial cell line-derived neurotrophic factor (GDNF) immunolabelling which has neurotrophic and neuroprotective effects on the survival of dopaminergic neurons. Furthermore, PB treatment was shown to protect CA1 and CA3 neurons in the hippocampus and dopaminergic neurons in the SN. DA levels in the SN were increased after PB treatment, leading to the improvement of motor function of PD rats. Conclusions: These results imply that PB prevents MPTP-induced neurotoxicity via its antioxidant activities and increases GDNF levels, which may contribute to the therapeutic strategy for PD.

Ischemic stroke is the most common type of stroke and poses a major global health challenge due to its high mortality and lasting disability impact. The onset and progression of ischemic stroke are largely linked to oxidative stress and inflammatory responses. Alpinetin, a natural flavonoid found in the ginger family, exhibits various pharmacological properties, including antioxidant and anti-inflammatory activities. In this study, the neuroprotective potential of alpinetin in attenuating oxidative stress and inflammation against cerebral ischemic stroke was evaluated. Ninety male Wistar rats were randomly assigned to the sham operation group, the Rt.MCAO group, the Rt.MCAO+piracetam group, and the Rt.MCAO+alpinetin groups (25, 50, and 100 mg/kg BW). Cerebral infarction size, neuronal density, and antioxidant and anti-inflammatory activities were measured. Three days of treatment with alpinetin markedly reduced the infarct volume by 30% compared to the Rt.MCAO+vehicle-treated group. Additionally, rats treated with alpinetin exhibited a significant increase in neuronal density in the cortex, as well as in the CA1 and CA3 regions of the hippocampus. Furthermore, treatment with alpinetin ameliorated both the Rt.MCAO-induced increase in malondialdehyde (MDA) activity and the Rt.MCAO-induced decrease in catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) activities in the cortex and hippocampus. Moreover, COX-2 and IL-6 protein levels were assessed using western blotting. The results showed that treatment with alpinetin (100 mg/kg BW) significantly reduced the expression levels of COX-2 and IL-6 in both the cortex and hippocampus. Our findings suggest that alpinetin significantly mitigates the effects of cerebral ischemia-induced brain damage through its antioxidant and anti-inflammatory properties and could potentially be developed as a therapeutic agent for stroke treatment.

Background: Long coronavirus disease (COVID) poses significant challenges for older adult patients, affecting their cardiopulmonary function and overall well-being. This study aimed to investigate the effects of slow deep breathing exercises on cardiopulmonary function, physical performance, biochemical markers, oxidative stress, and stress levels in older adult patients with long COVID. Methods: Sixty older adult patients with long COVID were randomly assigned to an exercise group of 30 patients and a control group of 30 patients. The exercise group engaged in slow deep breathing exercises for 30 minutes, five times a week over a period of 8 weeks, while the control group maintained their usual activities. Cardiovascular parameters, heart rate variability (HRV), respiratory muscle strength (RMS), pulmonary function tests (PFT), physical performance, biochemical and oxidative stress markers, and stress levels were assessed at baseline, 4 weeks, and 8 weeks. Data were analyzed using one-way repeated measures ANOVA. Results: The exercise group showed significant reductions in cardiovascular parameters (systolic and diastolic blood pressure, pulse pressure, mean arterial pressure, and heart rate). Additionally, RMS, PFT, and physical performance showed significant increases. Improvements were also observed in HRV, biochemical markers (fasting blood sugar and lipid profile), oxidative stress markers (catalase, superoxide dismutase, and malondialdehyde), and stress levels. In contrast, no significant changes were found in the control group. Conclusion: Slow deep breathing exercises, as a non-pharmacological intervention, significantly improve cardiopulmonary function, physical performance, and various health markers in older adult patients with long COVID. This approach provides a valuable and accessible therapeutic option for this population.

Background: One of the most common neurodegenerative diseases is Parkinson’s disease (PD); PD is characterized by a reduction of neurons containing dopamine in the substantia nigra (SN), which leads to a lack of dopamine (DA) in nigrostriatal pathways, resulting in motor function disorders. Oxidative stress is considered as one of the etiologies involved in dopaminergic neuronal loss. Thus, we aimed to investigate the neuroprotective effects of pinostrobin (PB), a bioflavonoid extracted from Boesenbergia rotunda with antioxidative activity in PD. Methods: Rats were treated with 40 mg/kg of PB for seven consecutive days before and after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD. After completing the experiment, the brains including SN and striatum were used for histological studies and biochemical assays. Results: PB treatment demonstrated a reduction of free radicals in the SN as indicated by significantly decreased MDA levels, whereas the antioxidative enzymes (SOD and GSH) were significantly increased. Furthermore, PB treatment significantly increased glial cell line-derived neurotrophic factor (GDNF) immunolabelling which has neurotrophic and neuroprotective effects on the survival of dopaminergic neurons. Furthermore, PB treatment was shown to protect CA1 and CA3 neurons in the hippocampus and dopaminergic neurons in the SN. DA levels in the SN were increased after PB treatment, leading to the improvement of motor function of PD rats. Conclusions: These results imply that PB prevents MPTP-induced neurotoxicity via its antioxidant activities and increases GDNF levels, which may contribute to the therapeutic strategy for PD.