"Sinew prescription correspondence" is the principle of selecting prescriptions for channel sinew diseases. On the basis of the theory of syndrome differentiation and treatment， the pulse manifestation corresponds to the channel sinew syndrome， which can improve the flexibility and standardization of clinical prescriptions. From the perspective of systematic dialectical sphygmology， this paper explains the dialectical relationship between channel sinew theory and pulse body elements， pulse wall elements， pulse elements and blood flow elements， and clarifies the internal relationship between pulse manifestation and prescriptions at the level of channel sinew disease. The prescription is derived from the method， while the method is established with the syndrome， and the prescription is unified by the method. According to the theory of "sinew prescription correspondence"， the treatment ideas of channel sinew diseases were analyzed from the perspective of channel sinew distribution， functional characteristics and structural changes. On this basis， the diagnosis of channel sinew disease and the application of prescriptions are expanded， and the research on the internal treatment and diagnosis mode of "pulse manifestation-channel sinew-zang fu （脏腑）" is prospected， so as to expand the differentiation and treatment methods of channel sinew theory.

Major depressive disorder (MDD) is a common mental disorder characterized by long-term low mood, anhedonia, and may even lead to suicidal behavior. The development and progression of MDD involves a range of pathological alterations in the central nervous system, including dysfunction of synaptic transmission, hyper-activation of neuroinflammation, and diminished neurogenesis. The transient receptor potential vanilloid 1 (TRPV1) channel is highly expressed in brain regions associated with depression, and can regulate physiological activities such as neuroinflammation, neurogenesis, and synaptic transmission efficacy. Hence, the TRPV1 channel should be implicated in the pathogenesis of depression and be considered as a promising candidate for antidepressant treatment. This paper provides an overview of the structure and function of TRPV1 channel, with a focus on elucidating the potential mechanism of action of TRPV1 channel in depression, and explores its research trajectory and development prospects in the context of depression therapy.

Major depressive disorder (MDD) is a common mental disorder characterized by long-term low mood, anhedonia, and may even lead to suicidal behavior. The development and progression of MDD involves a range of pathological alterations in the central nervous system, including dysfunction of synaptic transmission, hyper-activation of neuroinflammation, and diminished neurogenesis. The transient receptor potential vanilloid 1 (TRPV1) channel is highly expressed in brain regions associated with depression, and can regulate physiological activities such as neuroinflammation, neurogenesis, and synaptic transmission efficacy. Hence, the TRPV1 channel should be implicated in the pathogenesis of depression and be considered as a promising candidate for antidepressant treatment. This paper provides an overview of the structure and function of TRPV1 channel, with a focus on elucidating the potential mechanism of action of TRPV1 channel in depression, and explores its research trajectory and development prospects in the context of depression therapy.

Depressive disorder is a kind of mental disorder characterized by persistent and significant depressed mood, with complex etiology and high recurrence rate. At present, more precise and effective diagnostic and therapeutic approaches are still required. Increasing evidence suggests that hypoxia inducible factor-1 (HIF-1) and related pathways are involved in regulating the development and recovery of depression. HIF-1 enhances neuroplasticity, mitigates neuroinflammatory responses, alleviates oxidative stress, and modulates brain energy metabolism by influencing specific molecules associated with depression. This paper reviews pertinent domestic and international studies, examine the potential mechanisms of HIF-1 in the pathogenesis and progression of depression, and explore antidepressant treatment strategies targeting the HIF-1 signaling pathway. This article provides novel insights into elucidating the pathogenesis of depression and developing innovative therapeutic approaches.

Depressive disorder is a kind of mental disorder characterized by persistent and significant depressed mood, with complex etiology and high recurrence rate. At present, more precise and effective diagnostic and therapeutic approaches are still required. Increasing evidence suggests that hypoxia inducible factor-1 (HIF-1) and related pathways are involved in regulating the development and recovery of depression. HIF-1 enhances neuroplasticity, mitigates neuroinflammatory responses, alleviates oxidative stress, and modulates brain energy metabolism by influencing specific molecules associated with depression. This paper reviews pertinent domestic and international studies, examine the potential mechanisms of HIF-1 in the pathogenesis and progression of depression, and explore antidepressant treatment strategies targeting the HIF-1 signaling pathway. This article provides novel insights into elucidating the pathogenesis of depression and developing innovative therapeutic approaches.

Depression is a common debilitating disorder affecting over 300 million individuals worldwide, emphasizing the pressing need to develop novel treatment targets for this disorder. Nevertheless, the pathophysiology of this disorder remains incompletely elucidated, and the currently available antidepressant treatments are suboptimal in terms of their efficacy and delayed onset of action. Thus, identifying and exploring new therapeutic avenues is of paramount importance. Recent clinical and preclinical studies have demonstrated that numerous bitter taste receptor type 2 members (Tas2Rs) agonists, including epigallocatechin gallate (EGCG), resveratrol, caffeine, humulones, and berberine, can significantly alleviate depressive symptoms in both human patients and animal models of depression. However, the precise mechanisms underlying the antidepressant effects of Tas2Rs agonists remain largely unknown. Intriguingly, a growing body of evidence suggests that Tas2Rs agonists may modulate various signaling pathways and systems including neurotransmission, inflammation, brain-gut axis, and the blood-cerebrospinal fluid barrier, all of which are believed to be implicated in the pathophysiology of depression. Therefore, this review aims to provide a comprehensive overview of the potential mechanisms of Tas2Rs agonists in depression, It synthesizes current evidence regarding its involvement in neurotransmission, inflammation, brain-gut communication, blood-cerebrospinal fluid barrier function, and other relevant pathways. This review will not only provide a valuable foundation for future research on the therapeutic potential of Tas2Rs agonists for depressive disorders but also offer new insights into the understanding of the pathophysiology of depression and the development of novel treatment strategies for this disorder.

Major depressive disorder is a common mental disorder with high rate of disability and suicide rate, but its pathogenesis remains unclear. Numerous studies indicate that energy metabolism is impaired in patients with depression, with the changes in the expression of critical genes that regulate mitochondrial homeostasis (mitochondrial biogenesis, fusion and fission, and mitophagy). Mitochondrial dysfunction, leading to reduced ATP production, oxidative stress, and inflammation, plays a significant role in the onset and development of depression, but the mechanism is still uncertain, and conflicting research findings exist. This paper reviews the intrinsic connections and potential mechanism between mitochondrial homeostasis imbalance, dysfunction, and depression, from two aspects: mitochondrial imbalance and dysfunction. It also discusses the limitations of current research, providing insight into understanding the pathogenesis of depression and developing novel mitochondrial-targeted therapeutic strategies.

Depression is a common debilitating disorder affecting over 300 million individuals worldwide, emphasizing the pressing need to develop novel treatment targets for this disorder. Nevertheless, the pathophysiology of this disorder remains incompletely elucidated, and the currently available antidepressant treatments are suboptimal in terms of their efficacy and delayed onset of action. Thus, identifying and exploring new therapeutic avenues is of paramount importance. Recent clinical and preclinical studies have demonstrated that numerous bitter taste receptor type 2 members (Tas2Rs) agonists, including epigallocatechin gallate (EGCG), resveratrol, caffeine, humulones, and berberine, can significantly alleviate depressive symptoms in both human patients and animal models of depression. However, the precise mechanisms underlying the antidepressant effects of Tas2Rs agonists remain largely unknown. Intriguingly, a growing body of evidence suggests that Tas2Rs agonists may modulate various signaling pathways and systems including neurotransmission, inflammation, brain-gut axis, and the blood-cerebrospinal fluid barrier, all of which are believed to be implicated in the pathophysiology of depression. Therefore, this review aims to provide a comprehensive overview of the potential mechanisms of Tas2Rs agonists in depression, It synthesizes current evidence regarding its involvement in neurotransmission, inflammation, brain-gut communication, blood-cerebrospinal fluid barrier function, and other relevant pathways. This review will not only provide a valuable foundation for future research on the therapeutic potential of Tas2Rs agonists for depressive disorders but also offer new insights into the understanding of the pathophysiology of depression and the development of novel treatment strategies for this disorder.

Major depressive disorder is a common mental disorder with high rate of disability and suicide rate, but its pathogenesis remains unclear. Numerous studies indicate that energy metabolism is impaired in patients with depression, with the changes in the expression of critical genes that regulate mitochondrial homeostasis (mitochondrial biogenesis, fusion and fission, and mitophagy). Mitochondrial dysfunction, leading to reduced ATP production, oxidative stress, and inflammation, plays a significant role in the onset and development of depression, but the mechanism is still uncertain, and conflicting research findings exist. This paper reviews the intrinsic connections and potential mechanism between mitochondrial homeostasis imbalance, dysfunction, and depression, from two aspects: mitochondrial imbalance and dysfunction. It also discusses the limitations of current research, providing insight into understanding the pathogenesis of depression and developing novel mitochondrial-targeted therapeutic strategies.

Objective:To explore the effects of intrahippocampal injection of ferroptosis inducer Erastin on depressive- and anxiety-like behavior and the expression of ferroptosis-related proteins in rats.Methods:Forty 6-week-old healthy male Sprague-Dawley rats were randomly divided into five groups ( n=8/group): Control group, Erastin low-dose(200 ng/μL) group, Erastin medium-dose(400 ng/μL) group, Erastin high-dose group(600 ng/μL) and lipopolysaccharide (LPS, 10 μg/L) group.After the intrahippocampal injection of Erastin(2.5 μL per side), body weight, and behavioral tests, including sucrose preference test (SPT), forced swimming test (FST), open field test (OFT), and elevated plus maze (EPM), were performed to evaluate depressive- and anxiety-like phenotypes from the fourth day after injection.The levels of ferroptosis-related proteins and mRNA, including glutathione peroxidase 4 (GPX4), cyclo-oxygenase 2 (COX2), ferritin heavy polypeptide 1 (FTH1), long-chain fatty acyl-CoA synthetase 4 (ACSL4), solute carrier family 7 member 11 (SLC7A11) were measured using real-time quantitative PCR and Western blot analysis.SPSS 22.0 software was used for statistical analysis.One-Way ANOVA was used for multi-group comparison, and LSD was used for further pound-wise comparison. Results:(1)Body weight and behavioral tests: there were no statistically significant differences in baseline body weight and behavioral tests in these groups ( F=0.02-1.15, all P>0.05). After intrahippocampal injection, compared with the control group, medium-dose Erastin induced depression-like behaviors in rats more significantly, as indicated by reduced bodyweight ((245.20±5.24)g, (267.45±13.16)), sucrose preference in SPT ((32.14±8.51)%, (68.17±13.67)%), central time in OFT ((6.01±2.57)s, (16.49±7.21)s), percentage of time in open arm in EPM ((5.00±3.83)%, (19.63±5.91)%) and increased immobility time in FST ((37.00±7.58)s, (12.50±5.51)s) and percentage of time in closed arm in EPM ((89.43±4.77)%, (59.96±9.91)%), and there were statistically significant differences in these groups (all P<0.05). (2)The expression of ferroptosis-related indicators: after intrahippocampal injection, the expression of mRNA ( F=2.23, 8.37, 2.91, 7.60, 3.16, all P<0.05) and protein ( F=3.31, 40.13, 8.52, 3.70, 70.79, all P<0.05) of FTH1, GPX4, SLC7A11, COX2 and ACSL4 in hippocampus were statistically significant differences in the 5 groups.The mRNA and protein levels of FTH1, GPX4 and SLC7A11 in Erastin medium-dose group were lower than those in the control group (all P<0.05), while the mRNA and protein levels of COX2 and ACSL4 were higher than those in the control group (all P<0.05). Conclusion:Intrahippocampal microinjection of Erastin(400 ng/μL) can induce ferroptosis in hippocampus of rats and can also induce depressive-like behaviors in rats.