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Chronic inflammatory temporomandibular disorder (TMD) pain has a high prevalence, and available nonspecific treatments have adverse side effects. ECa 233, a standardized Centella asiatica extract, is highly anti-inflammatory and safe. We investigated its therapeutic effects by injecting complete Freund’s adjuvant (CFA) into right temporomandibular joint of mice and administering either ibuprofen or ECa 233 (30, 100, and 300 mg/kg) for 28 days. Inflammatory and nociceptive markers, bone density, and pain hypersensitivity were examined. CFA decreased ipsilateral bone density, suggesting inflammation localization, which ipsilaterally caused immediate calcitonin gene-related peptide elevation in the trigeminal ganglia (TG) and trigeminal subnucleus caudalis (TNC), followed by late increase of NaV1.7 in TG and of p-CREB and activation of microglia in TNC. Contralaterally, only p-CREB and activated microglia in TNC showed delayed increase. Pain hypersensitivity, which developed early ipsilaterally, but late contralaterally, was reduced by ibuprofen and ECa 233 (30 or 100 mg/kg). However, ibuprofen and only 100-mg/kg ECa 233 effectively mitigated marker elevation. This suggests 30-mg/kg ECa 233 was antinociceptive, whereas 100-mg/kg ECa 233 was both anti-inflammatory and antinociceptive. ECa 233 may be alternatively and safely used for treating chronic inflammatory TMD pain, showing an inverted U-shaped dose–response relationship with maximal effect at 100 mg/kg.

Permanent bilateral common carotid artery occlusion (2VO) in rodents induces chronic cerebral hypoperfusion, mimicking vascular dementia in elderly people. It causes inflammation and oxidative stress, leading to neuronal loss in the hippocampus, white matter injuries and impairments of spatial learning and memory. Thai Herbal Sahatsatara formula (STF) has anti-inflammatory and antioxidant actions which might protect neurons and white matter. This experiment was to investigate the possible protective effects of STF. Twenty-eight middle-aged male Wistar rats (12 months old) were divided into 4 groups: Sham+sterile water (SW), 2VO+SW, 2VO+STF300 and 2VO+STF1000. All animals daily received either SW, STF 300 mg/kg or STF 1000 mg/kg orally after 2VO induction until the end of the experiment. Spatial learning and memory test were examined after 2VO induction for 60 days whereas the numbers of hippocampal neurons and white matter changes in the corpus callosum were investigated after the end of the behavioral test. Chronic cerebral hypoperfusion significantly caused spatial learning and memory deficits and white matter injuries in the corpus callosum while the numbers of hippocampal neurons were not significantly affected. STF (1000 mg/kg) attenuated the impairments of spatial learning and learning flexibility and white matter injuries. This is the first study to demonstrate the ability of Sahatsatara formula to attenuate spatial learning and learning flexibility impairments after chronic cerebral hypoperfusion by protecting the white matter in the corpus callosum. The results support the potential application of Sahatsatara formula against chronic cerebral hypoperfusion.

Background Models of spinal cord injury (SCI) caused by weight-drop devices to cause contusion have been used extensively, and transient behavioral deficits after thoracic injury have been demonstrated. The severity of the injury caused by the device should be mild enough to allow recovery. Objective To determine whether our adapted weight-drop device with a small tip can effectively induce mild hemicontusion at the level of the fifth cervical vertebra. Methods We divided 15 adult male Sprague Dawley rats into groups of 5 for the following treatments: sham (SH, laminectomy only), mild (MSCI) or severe SCI (SSCI). Behavioral tests and histopathology were used before (day 1) and after the treatment on days 3, 7, 14, 21, 28, and 35 to assess the injury. Results Rats with SSCI showed a significant somatosensory deficit on days 3 and 7 compared with rats in the SH group, recovering by day 14. In a horizontal-ladder test of skilled locomotion, rats with SSCI showed a significant increase in error scores and percentage of total rungs used, and a decrease in the percentage of correct paw placement compared with rats in the SH group. There was greater recovery to normal paw placement by rats with MSCI than by rats with SSCI. These behavioral deficits were consistent with histopathology using hematoxylin and eosin counterstained Luxol fast blue, indicating the degree of injury and lesion area. Conclusions Mild hemicontusion caused by the adapted device can be used to evaluate SCI and provides a model with which to test the efficacy of translational therapies for SCI.