Evidence map›Paper›PMID 40938503›Full record

ArticleChinese journal of integrative medicine2026

Kai-Xin-San Has Antidepressant-Like Effect in Tricyclic Antidepressant Treatment Resistant Animal Model by Rebalancing Tryptophan Metabolism.

Lei Yao, Chao Chen, Rui Jing, Chao-Chen Wang, Yuan-Bo Wang, Xia Li, Li-Hua Mu, Hong Yin, Ping Liu, Yuan Hu

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Article in Chinese journal of integrative medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Lei YaoDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Chao ChenDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Rui JingDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Chao-Chen WangDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Yuan-Bo WangDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Xia LiDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Li-Hua MuDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Hong YinDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Ping LiuDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China.
Yuan HuDepartment of Pharmacy, Medical Supplier Center, Chinese PLA General Hospital, Beijing, 100853, China. huyuan1980619@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the effect of Kai-Xin-San (KXS), alone and in combination with imipramine (IMI), to ameliorate treatment-resistant depression (TRD) by normalizing tryptophan (TRP) metabolism.

methodsSixty Wistar rats were randomly divided into 6 groups using the lottery method (10 rats per group): control, adrenocorticotropic hormone (ACTH), IMI, KXS, KXS+IMI, and IMI+lithium (LIT). The control group received a vehicle solution, while the others were treated with ACTH (100 µg/d) for 14 days, and concurrently, KXS (365.4 mg/kg), IMI (10 mg/kg) and LIT (100 mg/kg) were administered to ACTH-treated rats for 15 days. The behavioral tests including forced swimming test (FST) and open-field test (OFT) were performed. The state of the hypothalamic-pituitary-adrenal (HPA) axis, the levels of key enzymes and critical products in TRP metabolism, the neuroinflammatory response and the expression of serotonin (5-HT) receptors, and the alterations in the glutamatergic signaling pathway were assessed. Furthermore, molecular docking was conducted to screen the major bioactive compounds in KXS.

resultsCompared with the ACTH group, KXS and KXS+IMI effectively deceased the immobility time in FST (P<0.01), increased the total distance, number of standing, center time, and center entries in OFT (P<0.05 or P<0.01), and attenuated the serum levels of ACTH and corticosterone (P<0.05 or P<0.01). KXS and KXS+IMI mitigated the disturbances in TRP catabolism by increasing kynurenine amino transferases, tryptophan hydroxylase, 5-HT and kynurenic acid levels while attenuating tryptophan-2,3-dioxygenase (TDO), kynurenine-3-monooxygenase, kynurenine/TRP ratio, and quinolinic acid in hippocampus or liver (P<0.05 or P<0.01). Additionally, KXS and KXS+IMI not only reduced the levels of neuroinflammation and serotonin 2A receptor, also rectified abnormalities in the glutamatergic system by activating brain-derived neurotrophic factor-mammalian target of rapamycin pathway in hippocampus of ACTH-challenged rats (P<0.05 or P<0.01). Moreover, molecular docking indicated that pachymic acid, ginsenoside Rg1 and tenuifolin could bind to TDO.

conclusionsThe therapeutic potential of KXS, especially combined with IMI, for TRD owed to its safeguarding effects on TRP metabolism. Pachymic acid, ginsenoside Rg1 and tenuifolin may be the primary contributors to these protective impacts of KXS.

Indexed as

Antidepressive AgentsDepressive Disorder, Treatment-ResistantDrugs, Chinese HerbalTryptophanAdrenocorticotropic HormoneAnimalsBehavior, AnimalDisease Models, AnimalHypothalamo-Hypophyseal SystemImipramineMaleMolecular Docking SimulationPituitary-Adrenal SystemRatsRats, WistarAdrenocorticotropic HormoneAntidepressive AgentsDrugs, Chinese HerbalImipramineKai-Xin-SanTryptophanChinese medicineKai-Xin-Sanmolecular dockingtherapeutic effecttreatment-resistant depressiontryptophan metabolic regulation

Identifiers

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.