RESUMEN
Allergic rhinitis(AR) is a common chronic inflammatory disease of the upper respiratory tract. Due to its high prevalence, high recurrence rate, and lack of a definitive cure, it is considered a global health issue by the World Health Organization. The pathogenesis of AR is complex and mainly involves B cells, helper T cells, eosinophils, basophils, macrophages, as well as the cytokines and inflammatory mediators they secrete. Clinical treatment primarily focuses on inhibiting inflammatory mediators such as histamine and leukotrienes. In recent years, active ingredients of animal-derived traditional Chinese medicine(TCM) have shown unique advantages and potential in AR treatment thanks to their high safety, specificity, selectivity, and biopotency. This study systematically reviewed the therapeutic effects and mechanisms of active ingredients and mixed extracts from animal-derived TCM, such as bovine spleen, honeycomb, bee venom, maggot, and human placenta, which have been shown by modern pharmacological research to regulate the immune function in AR, providing a reference for further exploration and clinical development of active ingredients from animal-derived TCM. Studies have found that the active ingredients from animal-derived TCM can produce definite therapeutic effects in AR by modulating multiple immune balances in the body, with great clinical prospects. However, their mechanisms of action still require further investigation, and the quality control techniques for effective ingredients need to be improved. Currently, the research on active ingredients from animal-derived TCM in China has adopted an interactive system consisting of "traditional medical experience-based research, bioinformatics and artificial intelligence predictions, and validation and development through new experimental techniques". Based on this system, animal-derived TCM can combine modern scientific and technological means to maximize the therapeutic effects of active ingredients and serve the clinical application of AR in a more efficient and innovative manner.
Asunto(s)
Medicamentos Herbarios Chinos , Poríferos , Rinitis Alérgica , Animales , Bovinos , Humanos , Medicina Tradicional China , Medicamentos Herbarios Chinos/farmacología , Medicamentos Herbarios Chinos/uso terapéutico , Inteligencia Artificial , Rinitis Alérgica/tratamiento farmacológico , Mediadores de InflamaciónRESUMEN
The Chinese herbal formula Tongluo Jiunao, containing the active components Panax notoginseng and Gardenia jasminoides, has recently been patented and is in use clinically. It is known to be neuroprotective in cerebral ischemia, but the underlying pathway remains poorly understood. In the present study, we established a rat model of cerebral ischemia by occlusion of the middle cerebral artery, and administered Tongluo Jiunao, a positive control (Xuesai Tong, containing Panax notoginseng) or saline intraperitoneally to investigate the pathway involved in the action of Tongluo Jiunao injection. 2,3,5-Triphenyltetrazolium chloride (TTC) staining showed that the cerebral infarct area was significantly smaller in model rats that received Tongluo Jiunao than in those that received saline. Enzyme-linked immunosorbent assay revealed significantly greater expression of neurotrophin 3 and growth-associated protein 43 in ischemic cerebral tissue, and serum levels of neurotrophin 3, in the Tongluo Jiunao group than in the saline group. The reverse transcription polymerase chain reaction and immunohistochemical staining showed that after treatment with Tongluo Jiunao or Xuesai Tong, tropomyosin-related kinase C gene expression and immunoreactivity were significantly elevated compared with saline, with the greatest expression observed after Tongluo Jiunao treatment. These findings suggest that Tongluo Jiunao injection exerts a neuroprotective effect in rats with cerebral ischemia by activating the neurotrophin 3/tropomyosin-related kinase C pathway.
RESUMEN
In view of the effective traditional Chinese medicine (TCM) in the treatment of clinical depression, the mechanism is not clear, this study attempts to research the cause of depression in a complex situation to lay the foundation for the next step of TCM curative effect evaluation. Based on the brain wave of 120 depression patients and 40 ordinary person, the change regulation of acetylcholine, dopamine, norepinephrine, depression neurotransmitters and excited neurotransmitters in the whole and various encephalic regions' multi-neurotransmitters of depression patients-serotonin are analysed by search of encephalo-telex (SET) system, which lays the foundation for the diagnosis of depression. The result showed that: contrased with the normal person group, the mean value of the six neurotransmitters in depression patients group are: (1) in the whole encephalic region of depression patients group the dopamine fall (P < 0.05), and in the double centralregions, right temporal region and right parietal region distinct fall (P < 0.01); (2) in the right temporal region of depression patients group the serotonin rise (P < 0.05); (3) in the right central region, left parietal region of depression patients group the acetylcholine fall (P < 0.05), left rear temporal region fall obviously (P < 0.01). The correlation research between antagonizing pairs of neurotransmitters and neurotransmitters: (1) the three antagonizing pairs of neurotransmitters-serotonin and dopamine, acetylcholine and norepinephrine, depression neurotransmitters and excited neurotransmitters, in ordinary person group and depression patients group are characterizeed by middle or strong negative correlation. Serotonin and dopamine, which are characterized by weak negative correlation in the right rear temporal region of ordinary person group, are characterized by strong negative correlation in the other encephalic regions and the whole encephalic (ordinary person group except the right rear temporal region: the range of [r] is [0.82, 0.92], P < 0.01)/(depression patients group:the range of [r] is [0.88, 0.94], P < 0.01); acetylcholine and norepinephrine, in the whole and various encephalic region are characterized by middle negative correlation(ordinary person group:the range of [r] is [0.39, 0.76], P < 0.01 or P < 0.05)/(depression patients group: the range of [Ir] is [0.56, 0.64], P < 0.01); depression neurotransmitters and excited neurotransmitters are characterized by middle strong negative correlation (ordinary person group: the range of [r] is [0.57, 0.80], P < 0.01)/(depression patients group: the range of [r] is [0.68, 0.78], P < 0.01). (2) The two neurotransmitters which are not antagonizing pairs of neurotransmitters, serotonin and excited neurotransmitters, or acetylcholine and depression neurotra-nsmitters, or dopamine and depression neurotransmitters in the various encephalic regions are characterized by weak negative correlation. Serotonin and excited neurotransmitters are characterizeed by weak negative correlation (ordinary person group: in the right central region, left parietal region, double front temporal regions, right rear temporal region, the range of [r] is [0.25, 0.50], P < 0.01 or P < 0.05)/(depression patients group: in the whole encephalic regions, double parietal regions, double occipital regions, right front temporal region, left central region, left frontal region, the range of [r] is [0.18, 0.37], P < 0.01 or P < 0.05); acetylcholine and depression, neurotransmitters are characterized by weak negative correlation (ordinary person group: in the double frontal regions, left parietal region, left front temporal region, right rear temporal region, the range of [r] is [0.31, 0.46], P < 0.01 or P < 0.05)/(depression patients group: in double rear temporal regions, right front temporal region, double occipital regions, left central region, the range of [r] is [0.20, 0.32] , P < 0.01 or P < 0.05); do-pamine and depression neurotransmitters are characterized by weak middle negative correlation (ordinary person group: in left parietal region, right central region, left frontal region, left occipital region, double front temporal regions, the range of [r] is [0.33, 0.68], P < 0.01 or P < 0.05)/(depression patients group: in the whole region and other various regions except the left frontal region, right central region, the range of Irl is [0.21, 0.34], P < 0.01 or P < 0.05). Dopamine and acetylcholine or norepinephrine and serotonin are characterized by weak positive correlation in all encephalic regions. Dopamine and acetylcholine are characterized by weak positive correlation (ordinary person group: in left frontal region, right parietal region, left front temporal region and left rear temporal region, the range of [r] is [0.37, 0.46], P < 0.01)/(depression patients group: in the whole region and the orther various regions except the double central regions, the range of [r] is [0.23, 0.5], P < 0.01 or P < 0.05); norepinephrine and serotonin are characterized by weak positive correlation (ordinary person group: in double front temporal regions, double rear temporal regions, right frontal region and left parietal region, the range of [r] is [0.34, 0.48], P < 0.01 or P < 0.05)/(depression patients group: in the whole and various regions, the range of [r] is [0.18, 0.42], P < 0.01). The main differences between the depression patients group and ordinary person group are: (1) In the whole regin, left frontal region and right central region of depression patients group, the six neurotransmitters all fall normally (P < 0.05). (2) The percent of dopamine falling or including dopamine falling, or including dopamine falling and serotonin rising in depression patients group increases. The percent of dopamine falling or including dopamine falling in the whole region, right frontal region, right central region increases (P < 0.01), such as dopamine decreasing, serotonin increasing dopamine decreasing, serotonin increasing acetylcholine decreasing dopamine decreasing, dopamine decreasing norepinephrine increasing depression neurotransmitters decreasing, serotonin increasing acetylcholine decreasing dopamine decreasing neurotransmitters increasing and so on. (3) The percent of acetylcholine falling, or including acetylcholine falling, or including acetylcholine falling and neurotransmitters (beta)-receptor)rising in depression patients group increases. The percent of acetylcholine falling, or including acetylcholine falling in the right temporal region, double central regions increases (P < 0.05 or P < 0.01), such as acetylcholine decreasing, acetylcholine decreasing neurotransmitters increaseng, acetylcholine decreasing neurotransmitters increasing depression neurotransmitters decreasing, serotonin increasing acetylcholine decreasing dopamine decreasing neurotransmitters increasing and so on. It's showed in research that depression patients' brain are characterized by multi-neurotransmitters abnormal, the synchronous change of multi-neurotransmitters has some certain regularities, which are not the simple linear relation. It's conformed that the three antagonizing pairs, neurotransmitters-serotonin and dopamine, acetylcholine and norepinephrine, depression eurotransmitters and excited neurotransmitters of ordinary person group and depression patients group, are both characterized by strong antagonizing relation, that the two neurotransmitters which are not antagonizing pairs of neurotransmitters are characterized by weak positive correlation or negative correlation, prompt maybe has the indirect causal relationship. And the change of six neurotransmitters in depression patients' various encephalic regions is rather complex. It's conformed preliminarily that the right frontal region and right central region are characterized by dopamine decreasing, acetylcholine decreasing, serotonin increasing dopamine decreasing, serotonin increasing acetylcholine decreasing dopamine decreasing, dopamine decreasing norepinephrine increasing excited neurotransmitters decreasing, serotonin increasing acetylcholine decreasing dopamine decreasing neurotransmitters increasing, acetylchoine decreasing neurotransmitters increasing, acetylcholine decreasing neurotransmitters increasing excited neurotransmitters decreasing and so on. Contrasted with the ordinary person group, the depression patients group have the notable difference.
Asunto(s)
Encéfalo/metabolismo , Depresión/metabolismo , Neurotransmisores/metabolismo , Acetilcolina/metabolismo , Adolescente , Adulto , Anciano , Estudios de Casos y Controles , Dopamina/metabolismo , Femenino , Humanos , Masculino , Persona de Mediana Edad , Norepinefrina/metabolismo , Serotonina/metabolismo , Adulto JovenRESUMEN
ETHNOPHARMACOLOGICAL RELEVANCE: Tong Luo Jiu Nao injection (TLJN), a modern Chinese formula based on Traditional Chinese Medicine theory, has been used to treat ischemic stroke and vascular dementia. TLJN belongs to the ethnopharmacological family of medicines. AIM OF THE STUDY: To investigate the protective effect of TLJN on oxygen-glucose deprivation (OGD) induced-injury of brain microvascular endothelial cells (BMECs). MATERIALS AND METHODS: The model of OGD was established in the primarily cultured BMECs. TLJN was added to the OGD-injured BMECs for 6h. A series of assays were used to detect the effects of TLJN on: (i) MIP-1ß content in BMECs conditioned media (CM) by ELISA; (ii) MIP-1ß protein expression in BMECs by western blotting and immunocytochemistry; (iii) the expression of CCR5, receptor of MIP-1ß, in BMECs by western blotting; (iv) the proliferative activity of microglial cells via the Cell Counting Kit-8 (CCK-8). RESULTS: Our results showed that the OGD-injured BMECs presented with large amounts of secretion and expression of MIP-1ß and up-regulation of CCR5. Also, the CM of OGD-injured BMECs remarkably increased the proliferative activity of microglial cells. The TLJN-treated BMECs exhibited a reduction of MIP-1ß content in BMECs-CM and a down-regulation of MIP-1ß and CCR5 expression. In addition, an inhibitory effect of CM of OGD-injured plus TLJN injection-treated BMECs on microglial proliferation was also found. CONCLUSION: TLJN reduced the expression of MIP-1ß and CCR5 in OGD-injured BMECs, and the CM of OGD-injured plus TLJN injection-treated BMECs inhibited the proliferative activity of microglial cells, suggesting the therapeutic potential of TLJN on ischemic cerebral vascular disease.
Asunto(s)
Encéfalo/irrigación sanguínea , Quimiocina CCL4/metabolismo , Medicamentos Herbarios Chinos/farmacología , Células Endoteliales/efectos de los fármacos , Glucosa/deficiencia , Microvasos/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Animales , Western Blotting , Hipoxia de la Célula , Proliferación Celular/efectos de los fármacos , Células Cultivadas , Medios de Cultivo Condicionados/metabolismo , Regulación hacia Abajo , Medicamentos Herbarios Chinos/administración & dosificación , Células Endoteliales/metabolismo , Células Endoteliales/patología , Ensayo de Inmunoadsorción Enzimática , Inmunohistoquímica , Inyecciones , Microglía/efectos de los fármacos , Microglía/patología , Microvasos/metabolismo , Microvasos/patología , Fármacos Neuroprotectores/administración & dosificación , Fitoterapia , Plantas Medicinales , Ratas , Ratas Sprague-Dawley , Receptores CCR5/metabolismo , Factores de TiempoRESUMEN
Neuronal survival can be influenced by activated microglia, but limited evidence exists on the effects of paracrine signaling from brain microvascular endothelial cells (BMECs) on microglial action. Therefore, we examined the effects of normal BMECs conditioned medium (BMECs-CM) on activated microglia induced by pro-inflammatory cytokine macrophage inflammatory protein-1beta (MIP-1ß), a chemokine that released from ischemic BMECs and has been proved to stimulate microglial proliferation. Our results showed that BMECs-CM inhibited the proliferation and transmigration of microglia induced by MIP-1ß. Moreover, BMECs-CM significantly suppressed the expression of the MIP-1ß receptor, CCR5, and the phosphorylation of p38 and JNK (P<0.05). These findings suggest that BMECs-CM could inhibit MIP-1ß-induced microglial activation. Future therapeutic strategies that prioritize the early recovery of BMECs could be beneficial for microglial inhibition and further increase neuronal survival.