Cerebral ischemia is a serious neurological disorder that can lead to high morbidity and mortality. Baicalin is a naturally bioactive flavonoid derived from Scutellaria baicalensis Georgi, which has neuroprotective activity. Baicalin exerts a neuroprotective effect against hypoxic ischemic injury. In this study, we investigated whether baicalin regulates specific proteins in the cerebral cortex of ischemic stroke animals. Middle cerebral artery occlusion (MCAO) surgery was performed to induce ischemic brain injury, and baicalin (30 mg/kg) or vehicle was injected into the abdominal cavity before MCAO surgery. Neurological behavior tests were performed 24 h after MCAO surgery and proteomics approach was performed using proteins extracted from cortical tissue. Two-dimensional electrophoresis analysis and MALDI-TOF were performed to identify the regulated protein by baicalin. MCAO damage caused severe behavioral disorders, but baicalin treatment improved these behavioral deficits. Baicalin also induced changes in the expression of various proteins in the cerebral cortex of MCAO animals. Proteins changed by baicalin administration are as follow: adenosylhomocysteinase, isocitrate dehydrogenase [NAD] subunit alpha, apolipoprotein A-I, Rab GDP dissociation inhibitor beta, eukaryotic initiation factor 4A, and mu-crystallin. These proteins were involved in metabolism and protein synthesis. The results of this study demonstrated the neuroprotective effects of baicalin by improving behavioral disorders caused by MCAO damage. The results also showed that baicalin regulates the expression of a variety of proteins involved in neuroprotective functions. Therefore, our findings provide evidence that baicalin plays a neuroprotective role in stroke animal models by regulating specific proteins.

Ischemic stroke is a high mortality disease that causes irreversible damage. Chlorogenic acid is a polyphenolic substance with neuroprotective properties. Bcl-2 family proteins perform a critical role in apoptosis process. Bcl-2 and Bcl-xL are anti-apoptotic proteins that prevent cell death, and Bax and Bad are pro-apoptotic proteins that promote apoptosis. We investigated whether chlorogenic acid modulates Bcl-2 family proteins during focal cerebral ischemia. We made a rat model of ischemic stroke by performing middle cerebral artery occlusion (MCAO). Chlorogenic acid (30 mg/kg) or phosphate-buffered saline was treated via intraperitoneal injection 2 hr before MCAO. Neurological behavioral tests were performed 24 hr after MCAO damage and cortical tissues were collected. Reverse transcription-PCR, Western blot, and immunofluorescence staining were performed to observe changes in Bcl-2 family proteins expression. MCAO-damage induced neurobehavioral disorders and chlorogenic acid alleviate these deficits. Bcl-2 and Bcl-xL expressions were decreased and Bax and Bad expressions were increased in MCAO animals. However, chlorogenic acid treatment attenuated the decrease of Bcl-2 and Bcl-xL and the increase of Bad and Bax due to MCAO surgery. Moreover, chlorogenic acid treatment attenuated MCAO-induced upregulation of caspase-3. These findings suggest that chlorogenic acid exerts neuroprotective effects against MCAO damage by regulating Bcl-2 family proteins including Bcl-2, Bcl-xL, Bax, and Bad.

Diabetes, a chronic hyperglycemic condition, is caused by insufficient insulin secretion or functional impairment. Long-term inadequate regulation of blood glucose levels or hyperglycemia can lead to various complications, such as retinopathy, nephropathy, and cardiovascular disease. Recent studies have explored the molecular mechanisms linking diabetes to bone loss and an increased susceptibility to fractures. This study reviews the characteristics and molecular mechanisms of diabetes-induced bone disease. Depending on the type of diabetes, changes in bone tissue vary. The molecular mechanisms responsible for bone loss in diabetes include the accumulation of advanced glycation end products (AGEs), upregulation of inflammatory cytokines, induction of oxidative stress, and deficiencies in insulin/IGF-1. In diabetes, alveolar bone loss results from complex interactions involving oral bacterial infections, host responses, and hyperglycemic stress in periodontal tissues. Therapeutic strategies for diabetes-induced bone loss may include blocking the AGEs signaling pathway, decreasing inflammatory cytokine activity, inhibiting reactive oxygen species generation and activity, and controlling glucose levels; however, further research is warranted.

Ischemic stroke is caused by a blockage of the cerebral artery, which leads to a severe neurological disorder. Chlorogenic acid is a phenolic acid found mainly in plants such as coffee beans, eggplants, and carrots. It exerts a neuroprotective effect against cerebral ischemic damage. Bcl-2 family protein is a representative apoptosis regulatory protein. Bcl-2 and Bcl-xL act as apoptosis inhibitors, while Bax and Bad act as apoptosis inducers.The interaction of Bcl-2 family protein plays an important role in determining cell fate. The aim of this study was to investigate whether chlorogenic acid modulates the interaction of Bcl-2 family proteins during ischemic injury. Middle cerebral artery occlusion (MCAO) surgery was performed to induce cerebral ischemia. Chlorogenic acid (30 mg/kg) or phosphate buffered saline was intraperitoneally injected to adult male rats 2 h after MCAO surgery. Neurobehavioral tests were performed to confirm the neuroprotective effect of chlorogenic acid 24 h after MCAO injury, and immunoprecipitation analysis was performed to investigate the interaction of Bcl-2 family protein. MCAO damage showed signs of severe neurological disorders, while chlorogenic acid improved these disorders. Results of immunoprecipitation analysis were as follows. Interaction between Bax and Bcl-2 or Bcl-xL was decreased in MCAO injury, chlorogenic acid prevents these decreases. In contrast to Bax, Interaction between Bad and Bcl-2 or Bcl-xL was increased in MCAO injury, chlorogenic acid prevents these increases. Furthermore, chlorogenic acid attenuated MCAO-induced increase of capase-9. In conclusion, our findings demonstrate that chlorogenic acid exerts a neuroprotective effect against cerebral ischemic injury by modulating interaction of Bcl-2 family proteins.

This study examines the rise of the Body Positive Movement on TikTok and its role as a form of online content activism influencing the fashion design and industry. Through a combination of literature review and case study methodology, the study explores the expression techniques and thematic types of Body Positive Movement on TikTok. Reviews of literature, previous studies, online articles, fashion journals, and relevant search terms on TikTok informed a definition of Body Positive Movement and an analysis of its formation and rise. The research findings confirm the impact TikTok content on Body Positive Movement has on the fashion industry in addressing external factors (i.e., ‘Appearance’, ‘Race’, ‘Aging’, ‘Physical Disability’) and intrinsic factors (i.e., ‘Acceptance of Diversity’, ‘Self-Esteem’, ‘Rejection of Stereotypes’, ‘Appropriate Representation’, ‘Information Provision’). The key external factor , ‘Appearance’, includes subcategories such as ‘Body Shape’, ‘Body Hair’, ‘Skin’, and ‘Facial Features’. TikTok content creators on fashion creatively combine music, emojis, and visual storytelling to exhibit positive self-perception concerning these factors. A significant finding of the study is that short clips predominantly manifesting external factors differentiate into informative or enlightening videos associated with intrinsic factors. The study underscores Body Positive Movement's important influence on the fashion industry from design to presentation.

Hongjam is a natural health food that has been shown to have various health-promoting effects, but studies on immunity enhancement have not been done so far. In this study, we investigated whether HongJam extracts could be enhancing innate immunity by protomoting proliferatin of macrophages and their phagocytic or pinocytic abilities to pathogens. (Grant No. PJ017024022023)

Immunity is largely divided into innate immunity and adaptive immunity. We conducted a study using HongJam extract to confirm its innate immunity-enhancing effect. Our data using Natural Killer (NK) cells, which play an important role in innate immunity, confirmed that HongJam extract promotes the proliferation of NK cells and also enhances the function of NK cells to attack and destroy cancer cells. (Grant No. PJ017024022023)

The enzyme digestion of foods is known to have certain advantages, such as enhancing health improvement functions of functional foods. In this study, we investigated whether the memory enhancement effects of HongJam could be enhanced by enzymatic digestions. We found that enzyme digested HJ had more enhanced functionality than undigested HJ. We also found the molecular basis of memory enhancement by performing various biochemical and molecular biological experiments. (Grant No. PJ016908032023)

Recently, the occurrence of the fall webworm, one of the foreign invasive pests, is rapidly increasing due to the increase in average annual temperature due to global climate changes. In this study, we are presenting diverse eco-friendly technologies to control the fall webworm. (Grant No. PJ014845032023).

Ischemic stroke leads to severe brain damage and high mortality. Chlorogenic acid is a phenolic compound known to have neuroprotective properties. Bcl-2 family protein plays an important role in the regulation of apoptosis. We investigated whether chlorogenic acid exerts neuroprotective effects against ischemic injury by modulating Bcl-2 and Bax proteins. Middle cerebral artery occlusion (MCAO) was performed to induce cerebral ischemia and rats were injected intraperitoneally with phosphate buffered saline or chlorogenic acid (30 mg/kg) for 2 h after MCAO. Cortical tissues were collected 24 h after MCAO injury and reverse transcription-quantitative real time polymerase chain reaction and Western blot analyses were performed to investigate the expression of Bcl-2 and Bax. The regulation of Bcl-2 and Bax proteins by chlorogenic acid during glutamateinduced cell damage were examined. Cells were collected at 24 h after administration of glutamate (5 mM) and chlorogenic acid (10, 30, 50 μM). These results showed a decrease in Bcl-2 expression and an increase in Bax expression in MCAO animals, but chlorogenic acid treatment alleviated these changes by MCAO damage. Glutamate significantly reduced cell viability, and chlorogenic acid treatment alleviated this reduction in a dose-dependent manner. Glutamate induced a decrease in Bcl-2 expression and an increase in Bax expression, but chlorogenic acid treatment alleviated these changes. We found that chlorogenic acid alleviates changes in the expression of Bcl-2 and Bax proteins induced by brain injury. Therefore, our findings provide an evidence that chlorogenic acid has neuroprotective effects against MCAO damage by modulating Bcl-2 and Bax proteins.

Ischemic stroke causes severe neuronal damage. Chlorogenic acid is a phenolic substance present in fruits and coffee. It also exerts neuroprotective effects against various brain injuries. The 14-3-3 family protein perform a variety of functions including metabolism, signal transduction, cell differentiation, and apoptosis. The purpose of this study is to investigate whether chlorogenic acid regulates the expression of 14-3-3 protein in stroke animal models. Ischemic stroke was induced by middle cerebral artery occlusion (MCAO) surgery. Phosphate buffered saline (PBS) or chlorogenic acid (30 mg/kg) were intraperitoneally injected to adult male rats 2 h before MCAO surgery. Adhesive-removal test was performed 24 h after MCAO surgery and cerebral cortical tissues were collected for further study. MCAO damage caused severe neurological impairment and chlorogenic acid treatment ameliorated this disorder. Our proteomic approach showed a decrease in 14-3-3 expression in MCAO animals with PBS. The decrease in 14-3-3 expression alleviated in MCAO animal with chlorogenic acid. We confirmed changes in various 14-3-3 protein isoforms, including beta/alpha, zeta/delta, gamma, epsilon, eta, and tau through reverse transcription-PCR. These results explained that chlorogenic acid regulates the expression of 14-3-3 protein in MCAO-induced cerebral ischemia. 14-3-3 is considered to be an important protein for cell survival through binding to pro-apoptotic proteins. The maintenance of 14-3-3 levels is an important event in neuroprotection against ischemic injury. Therefore, we can demonstrate that the 14-3-3 protein contributes to the neuroprotective effect of chlorogenic acid in stroke animal models.

Ischemic stroke causes brain damage and neuronal cell death by depriving oxygen and nutrients and releasing excessive levels of glutamate and intracellular calcium. Epigallocatechin gallate (EGCG) is a polyphenolic compound present in green tea. It has antioxidant, anti-inflammatory, and neuroprotective effects. Hippocalcin is a calcium binding protein that regulates calcium concentration, neuronal differentiation, neuronal excitability, and neuronal cell death. In this study, we investigated whether EGCG regulates the expression of hippocalcin in neurons and astrocytes after focal cerebral ischemia. Cerebral ischemia was induced by meddle cerebral artery occlusion (MCAO). EGCG (50 mg/kg) or PBS was injected into the abdominal cavity just before MCAO surgery. Neurobehavioral tests were performed to evaluate the effect of EGCG on neurological behavioral deficits 24 h after MCAO surgery. Immunofluorescence staining was performed to evaluate the positive response to hippocalcin in the cerebral cortex after MCAO surgery. We also detected the positive reactions of neuronal nuclear protein (NeuN) and glial fibrillary acidic protein (GFAP) as markers of neuron and astrocyte, respectively. MCAO caused severe neurological impairment and EGCG treatment attenuated these impairments. MCAO damage reduced the number of NeuN-positive cells and increased the number of GFAP-positive cells. This result indicates a decrease in neurons and an increase in astrocytes. However, EGCG alleviated these changes caused by MCAO damage. MCAO reduced the number of hippocalcin-positive cells in neurons and astrocytes, and EGCG treatment attenuated these reductions. Hippocalcin exerts neuroprotective effect through regulating intracellular calcium concentration. In conclusion, EGCG regulates the expression of hippocalcin in neurons and astrocytes and has neuroprotective effects in focal cerebral ischemia.