The pain matrix including the anterior cingulate cortex (ACC) mediates not only first person pain experience but also empathy for others' pain. It remains unknown, however, whether empathic neural responses of the pain matrix are modulated by racial in-group/out-group relationship. Using functional magnetic resonance imaging we demonstrate that, whereas painful stimulations applied to racial in-group faces induced increased activations in the ACC and inferior frontal/insula cortex in both Caucasians and Chinese, the empathic neural response in the ACC decreased significantly when participants viewed faces of other races. Our findings uncover neural mechanisms of an empathic bias toward racial in-group members.

No abstract

Recent neuroimaging research has shown increased neural activity in adults in response to perceived pain in same-race versus other-race individuals. Moreover, manipulations of cognitive strategies and intergroup relationships in laboratory can significantly reduce the racial bias in empathic neural responses by increasing the neural activity to perceived pain in other-race individuals. The current study further investigated whether real-life cultural experiences with other-race individuals can reduce the racial bias in empathic neural responses to others' suffering. Using functional magnetic resonance imaging, we scanned 20 Chinese adults who were brought up in Western countries (United States, United Kingdom, and Canada) where Caucasians consist of the majority of population. Participants viewed video clips in which either Asian or Caucasian models received painful or non-painful stimulations. We found that the neural activity in the pain matrix including the anterior cingulate cortex, anterior insula, inferior frontal cortex and somatosensory cortex was significantly increased in response to painful versus nonpainful stimuli applied to both Asian and Caucasian models. Moreover, these empathic neural responses to Asian and Caucasian models did not differ significantly and were positively correlated with each other. Our results indicate that cultural experiences with racial out-group members may increase the neural responses to the suffering of other-race individuals and thus reduce the racial bias in empathy.

Objective: Sarcopenia causes loss of skeletal muscle and function, thus seriously affecting the physical function and quality of life in the elderly. This article discusses the specific molecular mechanism and ameliorating effects of Tudangshen (TDS) on sarcopenia in elderly rats with type 2 diabetes mellitus (T2DM).Methods: Elderly Sprague-Dawley (SD) rats were randomly selected and fed with a high-fat diet combined with an intraperitoneal injection of streptozotocin to establish T2DM model. The model rats were stratified and randomly divided into the model group, metformin group, TDS high-dose group, TDS medium-dose group, and TDS low-dose group according to blood glucose combined with body weight, and the same batch of old SD rats was set as the normal control group. The effects of TDS in an elderly T2DM sarcopenia rat model were evaluated by observing the body positions of the rats, analyzing blood biochemistry, testing exercise capacity, and pathologically staining sectioned gastrocnemius muscle tissues. The molecular mechanisms of the effects were analyzed using quantitative real-time polymerase chain reaction and western blotting.Results: TDS has no statistically significant effect on blood glucose, insulin and glycosylated serum protein in aged rats with T2DM, but it can reduce levels of glycosylated serum protein, total cholesterol, triglycerides, and low-density lipoprotein; it improves pathological changes in rat gastrocnemius muscle tissues, and increases muscle cell activity in elderly rats with T2DM and sarcopenia. TDS also promoted the upregulation of the expression of mammalian target of rapamycin (mTOR)/protein kinase B (PKB/AKT)/phosphatidylinositol 3-kinase (PI3K)/ribosomal protein S6 kinase/eukaryotic initiation factor 4E binding rotein1 mRNA in rats and triggered an increase in corresponding protein levels.Conclusions: TDS alleviated muscle decline in elderly rats with T2DM by activating the PI3K/AKT/mTOR signaling pathway and regulating the synthesis of corresponding proteins.