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3.
Biomed Pharmacother ; 139: 111580, 2021 Jul.
Article in English | MEDLINE | ID: mdl-33857914

ABSTRACT

Qing-Chang-Hua-Shi (QCHS) is a Chinese herbal formula, which is composed of 11 herbs. Studies have also shown that QCHS granules can alleviate colitis in animal models by preventing inflammatory responses and suppressing apoptosis through the MEK/ERK signaling pathway. To determine the efficacy and safety of QCHS granules in patients with moderately active UC. We performed a multicenter, randomized, placebo-controlled, double-blind study of patients with moderately active UC who did not respond to 4 weeks of mesalazine therapy at the maximum dose. Patients were randomly assigned to groups and administered QCHS granules (125 g/day, n = 59) or an identical placebo, which was similar to the QCHS granules in color and taste (125 g/day, n = 60), with continued 5-ASA 4 g/d therapy for 12 weeks. The primary outcome was the rate of clinical response and clinical remission at week 12. The secondary outcomes were health-related quality of life, endoscopic response rate, and mucosal healing rate. Any changes in mucus/bloody stool and diarrhea were recorded. Out of the 119 enrolled patients at 10 different centers in China, 102 patients completed the trial. Clinical remission and clinical response were seen in 31.48% and 92.59% of QCHS-treated patients, and 12.50% and 72.92% of placebo-treated patients, respectively. There was a significant difference between the two treatment groups. More patients receiving QCHS granules vs. placebo achieved remission of mucus/bloody stool (70.37% vs. 47.92%, P = 0.0361). Adverse event rates were similar (QCHS granules 38.33%; placebo 25.42%). In conclusion, QCHS granules were superior to the placebo in introducing clinical remission and mucosal healing, as well as in relieving mucus/blood stool in patients with moderately active and 5-ASA-refractory UC.


Subject(s)
Anti-Ulcer Agents/therapeutic use , Colitis, Ulcerative/drug therapy , Drugs, Chinese Herbal/therapeutic use , Adult , Anti-Ulcer Agents/adverse effects , Colitis, Ulcerative/pathology , Colitis, Ulcerative/psychology , Double-Blind Method , Drugs, Chinese Herbal/adverse effects , Female , Humans , Intestinal Mucosa/pathology , Male , Mesalamine/therapeutic use , Middle Aged , Prospective Studies , Quality of Life , Sulfasalazine/therapeutic use , Treatment Outcome
4.
Trials ; 22(1): 55, 2021 Jan 13.
Article in English | MEDLINE | ID: mdl-33441157

ABSTRACT

BACKGROUND: Ulcerative colitis (UC) is an intestinal inflammatory disease characterized by inflammation of the colonic mucosa. With unknown pathogenesis, it has become a chronic lifetime disorder worldwide. In patients with moderately active UC, several therapies (e.g., aminosalicylates, corticosteroids, immunosuppressants, and biologics) are recommended for induction (or maintenance) of remission. Given the side effects and disease burden, it is difficult for most patients to achieve ideal treatment goals in clinical practice. Chinese herbal medicine (CHM), as a complementary therapy, has been widely used in the management of UC in China. Qing-Chang-Hua-Shi granule (QCHS) is a classical Chinese herbal formula. Our preliminary study suggested that the QCHS decoction has a significant effect on patients with moderately active UC. However, its effectiveness and safety has not been evaluated convincingly. Therefore, we designed this protocol to investigate the efficacy of QCHS granule for moderately active UC. METHODS: This is a multicenter, randomized, double-blind, placebo-controlled, superiority trial. A total of 120 patients with moderately active UC will be recruited from 10 hospitals in China. Each eligible participant will be randomly assigned to receive QCHS granule or placebo for 12 weeks. Both groups will be given basic treatment with mesalazine (4 g/day). The primary outcomes are the clinical response (remission) rate. The secondary outcomes are health-related quality of life, endoscopic response rate, mucosal healing rate, and inflammatory markers (e.g., fecal calprotectin and CRP). The whole study period will last 36 weeks, including 24 weeks follow-up time. According to the intention-to-treat principle, variables will be assessed at 2, 4, 6, 8, 10, and 12 weeks after study commencement. DISCUSSION: This is the first randomized controlled clinical study protocol regarding Chinese herbal extract granules in the management of moderately active UC. We aim to investigate the superiority of QCHS granules over placebo in terms of induction of remission. If the trial shows significant benefits of QCHS granules, it will help clinical practitioners, UC patients, and policymakers make more informed choices in the decision-making. TRIAL REGISTRATION: Chinese Clinical Trial Registry ChiCTR-IOR-14005554 . Registered on 27 November 2014.


Subject(s)
Colitis, Ulcerative , Drugs, Chinese Herbal , China , Colitis, Ulcerative/diagnosis , Colitis, Ulcerative/drug therapy , Double-Blind Method , Drugs, Chinese Herbal/adverse effects , Humans , Mesalamine/adverse effects , Multicenter Studies as Topic , Quality of Life , Randomized Controlled Trials as Topic , Treatment Outcome
5.
BMC Complement Med Ther ; 20(1): 291, 2020 Sep 23.
Article in English | MEDLINE | ID: mdl-32967687

ABSTRACT

BACKGROUND: The balance between T helper 17 (Th17) cells and regulatory T cells (Tregs) is involved in immunological tolerance. Destruction of immunological tolerance by dendritic cell (DC)-mediated T cells is involved in the pathogenesis of ulcerative colitis (UC). Qingchang Huashi granule (QCHS) has been confirmed in the treatment of UC involved by inhibiting the activation of DCs. The aim of this study was to investigate the mechanism through which QCHS restores the Th17/Treg balance by modulating DCs in the treatment of UC. METHODS: The effects of QCHS on Th17 cells, Tregs and DCs were detected in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis model. Furthermore, we injected QCHS-treated DCs into colitis model to test whether QCHS modulates the Th17/Treg balance via DCs. Tregs and Th17 cells were analyzed by FACS. IL-10, IL-17, and Foxp3 were measured by ELISA, Western blot and qRT-PCR. RESULTS: Both QCHS and QCHS-treated DCs improved colonic histopathology, diminished Th17 cell differentiation and inhibited IL-17 production while promoting CD4+CD25+Foxp3+ Treg differentiation and augmenting IL-10 and Foxp3 expression in colitis mice. Additionally, QCHS reduced CD86 and MHC-II expression on DCs, decreased IL-12 production ex vivo and restored the Th17/Treg ratio in the colitis model. CONCLUSION: The findings of this study indicate that QCHS ameliorates TNBS-induced colitis by restoring the DC-mediated Th17/Treg balance.


Subject(s)
Colitis, Ulcerative/drug therapy , Colitis, Ulcerative/immunology , Dendritic Cells/immunology , Drugs, Chinese Herbal/pharmacology , T-Lymphocytes, Regulatory/immunology , Th17 Cells/immunology , Animals , Cell Differentiation , Disease Models, Animal , Male , Mice , Mice, Inbred C57BL , Trinitrobenzenesulfonic Acid
6.
Exp Ther Med ; 20(1): 581-590, 2020 Jul.
Article in English | MEDLINE | ID: mdl-32537016

ABSTRACT

Inflammatory bowel diseases (IBDs) are chronic immunological disorders of the intestinal tract characterized by persistent inflammation. Baicalin, a type of flavonoid, has exhibited a wide range of pharmacological activities, including immunomodulation and anti-inflammation. However, little is known about the therapeutic role of baicalin in IBD. The aim of the present study was to ascertain whether baicalin could be a therapeutic drug of IBD and investigate its specific mechanisms. In the present study, the results revealed that baicalin not only significantly alleviated TNBS-induced colitis by reducing the release of IL-6, TNF-α and IL-1ß and increasing the level of IL-10, but promoted the expression of tight-junction proteins ZO-1 and ß-catenin, which may have been achieved by blockage of the PI3K/AKT signaling pathway. In vitro, the results demonstrated that baicalin clearly inhibited the release of TNF-α, IL-6 and IL-1ß and promoted the expression of IL-10 in LPS-induced HT-29 cells, and significantly decreased LPS-induced HT-29 cell apoptosis by blockage of the PI3K/AKT signaling pathway. In conclusion, the present research revealed for the first time that baicalin acted as a therapeutic drug in IBD by suppression of the PI3K/AKT signaling pathway.

7.
Zhongguo Zhen Jiu ; 40(5): 557-64, 2020 May 12.
Article in Chinese | MEDLINE | ID: mdl-32394667

ABSTRACT

The data mining technology was used to explore the acupoint selection rules for reflux esophagitis (RE), so as to provide references of clinical acupuncture for RE. The clinical literature of acupuncture for RE published before June 2019 was searched in Chinese journal full-text database (CNKI), SinoMed, Wanfang and VIP databases. The literature was selected according to the inclusion and exclusion criteria and acupoint prescriptions were extracted. The software of IBM SPSS Statistics 23.0 and Clementine 12.0 were used for descriptive analysis and association analysis. A total of 46 articles were selected and 60 acupoint prescriptions were extracted. The descriptive analysis indicated that the top five acupoints used for RE were Zhongwan (CV 12), Zusanli (ST 36), Weishu (BL 21), Neiguan (PC 6) and Gongsun (SP 4). The conception vessel, bladder meridian and stomach meridian were the most commonly selected meridians. In terms of specific acupoints, the crossing points, the front-mu points and five-shu points were mainly selected, and the acupoints were mainly distributed in limbs and chest-abdomen. The core acupoint combination for RE was "Zhongwan (CV 12) and Zusanli (ST 36)" and the core prescription was "Zhongwan (CV 12), Zusanli (ST 36), Weishu (BL 21) and Neiguan (PC 6)".


Subject(s)
Acupuncture Points , Acupuncture Therapy , Esophagitis, Peptic/therapy , Meridians , Data Mining , Humans
8.
Biomed Pharmacother ; 116: 108967, 2019 Aug.
Article in English | MEDLINE | ID: mdl-31102937

ABSTRACT

Ulcerative colitis (UC), a bowel disease with significant morbidity, is associated with inflammation. In this study, the effect of Qingchang Huashi granule (QCHS) on UC and its underlying mechanisms were explored using both animal and cell culture experiments. A rat UC model was induced with trinitro-benzene-sulfonic acid (TNBS), concentrations of the cytokines IL-1α, IL-6, IL-8, IL-1ß, and TNF-α were significantly up-regulated and the concentrations of IL-4, IL-10, and IL-13 were significantly down-regulated compared with the control group (P < 0.05). In contrast, the QCHS and salicylazosulfapyridine (SASP) groups reversed these modulations (P < 0.05). A UC cell model in HT-29 cells was generated using TNF-α combined with lipopolysaccharide treatment. Cells treated with QCHS were used to investigate the possible mechanisms. The expression of apoptosis-related proteins, including Bax/Bcl-2, caspase-3, caspase-9, Fas/Fas-L, and Rafl in the QCHS and SASP groups, were significantly lower than that in the control group in both animal and cell experiments (P < 0.05). In addition, the in vitro results indicate changes in these indicators mediate the MEK/ERK signaling pathways via SGK1. Our results suggested that QCHS could be beneficial in preventing UC progression as an alternative drug for UC treatment.


Subject(s)
Colitis, Ulcerative/drug therapy , Colitis, Ulcerative/enzymology , Drugs, Chinese Herbal/therapeutic use , Inflammation/pathology , MAP Kinase Signaling System/drug effects , Models, Biological , Animals , Apoptosis/drug effects , Biomarkers/metabolism , Colitis, Ulcerative/pathology , Colon/drug effects , Colon/pathology , Cytokines/metabolism , Disease Models, Animal , Drugs, Chinese Herbal/pharmacology , Female , Gene Silencing , HT29 Cells , Humans , Immediate-Early Proteins/metabolism , Lipopolysaccharides , Male , Protein Serine-Threonine Kinases/metabolism , RNA, Messenger/genetics , RNA, Messenger/metabolism , Rats, Sprague-Dawley
9.
Medicine (Baltimore) ; 98(9): e14622, 2019 Mar.
Article in English | MEDLINE | ID: mdl-30817579

ABSTRACT

RATIONALE: Inflammatory bowel disease (IBD), including Crohn disease (CD) and ulcerative colitis (UC), is characterized by chronic inflammatory condition and immunological abnormalities, which probably develop into venous thromboembolic events (VTEs). VTE in IBD patients mostly occurs at deep venous thrombosis (DVT) and pulmonary embolism (PE). The complications are extremely important in clinical practice considering the high mortality rate. Hence, an early diagnosis of IBD and the control of complications play an important role in therapy of thromboembolic events (TEEs). PATIENT CONCERNS: Case 1 was a 31-year-old man with chronic UC who presented with signs of thromboembolism. Case 2 was a 43-year-old woman with CD complicated by fistulas. DIAGNOSES: Computed tomography (CT) and digital subtraction angiography (DSA) of the patient (case 1) suggested a thrombus in cerebral vein. The patient (case 2) developed acute ischemia of her right arm; B ultrasonography revealed a thrombus in the distal of the right subclavian artery accompanied by stenosis. INTERVENTIONS: To lower blood viscosity and overcome the risk of deep thrombosis, the patient (case 1) was treated with a combination of low-molecular-weight heparin and dextran as anticoagulation. For the patient (case 2), anticoagulation treatment with 75 mg qd clopidogrel (plavix) and 1.25 mg qd warfarin was performed. OUTCOMES: In both patients, no further TEE occurred during follow-up 1 year and one and a half years, respectively. LESSONS: It is important to pay attention to IBD patients especially those with high coagulation state.


Subject(s)
Cerebral Veins , Colitis, Ulcerative/complications , Crohn Disease/complications , Venous Thromboembolism/etiology , Venous Thrombosis/etiology , Adult , Female , Humans , Intestinal Fistula/etiology , Male
10.
Int Immunopharmacol ; 68: 242-251, 2019 Mar.
Article in English | MEDLINE | ID: mdl-30743078

ABSTRACT

BACKGROUND: Berberine hydrochloride is one the effective compound among Rhizoma Coptidis, Cortex Phellodendri, and other plants. There are several clinical functions of berberine hydrochloride including anti-inflammation, antitumor and immunoregulatory. However, the anti-inflammatory of berberine hydrochloride in ulcerative colitis is barely understood. In this study, we aimed to explore the effects of berberine hydrochloride on dextran sulfate sodium (DSS)-induced rats model of ulcerative colitis. METHODS: The severity of colitis were measured by body weight, survial rate, colon length and disease activity index (DAI) score. The cytokines expression include IL-1, IL-1ß, IL-4, IL-6, IL-10, IL-12, TNF-α, TGF-ß and IFN-γ were performed by RT-PCR and ELISA. Signaling pathway proteins such as p-STAT3, STAT3, p-NF-κB p65 and NF-κB p65 were analyzed by western blot and immunofluorescence. The proteins expression of tight junction were explored using western blotting and immunohistochemistry. RESULT: Rats were administered berberine hydrochloride showed less weight loss and longer colon length than the DSS-induced group. The expression of IL-1, IL-1ß, IL-6, IL-12, TNF-α, TGF-ß and IFN-γ were suppressed, yet the expression of IL-4 and IL-10 were up-regulated by berberine hydrochloride and sulphasalazine treatment compared to the model group. Meanwhile, treatment with berberine hydrochloride effectively increased the expression of SIgA and decreased the expression of iNOS, MPO, MDA. In terms of the biochemical analyses, the results showed that the expression of p-STAT3 was signifcantly increased, while the expression of p-NF-κB (p65) was suppressed compared to the model group via western blot and immunofluorescence analysis. CONCLUSIONS: Berberine hydrochloride has beneficial effects in UC. The possible mechanism of anti-inflammatory response by berberine hydrochloride may involve in the blocking of the IL-6/STAT3/NF-κB signaling pathway. Collectively, these fndings provide evidence that berberine hydrochloride might be a useful herb medicine and serve as a promising novel therapy in the treatment of UC in humans.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Berberine/therapeutic use , Colitis, Ulcerative/drug therapy , Animals , Anti-Inflammatory Agents/pharmacology , Berberine/pharmacology , Colitis, Ulcerative/chemically induced , Colitis, Ulcerative/immunology , Cytokines/immunology , Dextran Sulfate , Disease Models, Animal , Male , NF-kappa B/immunology , Rats, Wistar , STAT3 Transcription Factor/immunology
11.
Int Immunopharmacol ; 67: 129-137, 2019 Feb.
Article in English | MEDLINE | ID: mdl-30544066

ABSTRACT

Gallic acid (GA), as an active component, has been found in many fruits and plants, and it exhibits potential protective effects, such as anti-inflammatory, antioxidant, antiviral and anticancer. However, the effects of GA on ulcerative colitis (UC) remain unknown. The purpose of this study was to investigate the effects of GA on IL-1ß-induced HIEC-6 cells and TNBS-induced UC in mice. Various biochemical analyses including proliferation and apoptosis were assessed in HIEC-6 cells. In addition, body weight of mice, the level of cytokines and histological changes were utilized to analyze the GA protecting mice with UC. Our results showed that administration of GA significantly increased the expressions of IL-4, and IL-10, while down-regulated IL-1, IL-6, IL-12, IL-17, IL-23, TGF-ß and TNF-α expressions compared with a model control group in vitro and in vivo. Moreover, flow cytometry and TUNEL analysis revealed that administration of GA significantly inhibited the apoptosis of HIEC-6 cells and mics in UC. Furthermore, pretreatment with GA obviously reversed the decrease in body weight, increase in colon weight, and attenuated the histological changes derived from UC. In addition, western blot analysis demonstrated that GA efficiently suppressed NF-κB signaling pathway in TNBS-induced UC. In conclusion, the findings of this study demonstrated that GA plays an anti-inflammatory role in UC via inhibiting NF-κB pathway.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Colitis, Ulcerative/drug therapy , Gallic Acid/therapeutic use , Inflammation/drug therapy , Intestine, Small/pathology , Animals , Apoptosis , Cell Line , Cell Proliferation , Colitis, Ulcerative/chemically induced , Cytokines/metabolism , Disease Models, Animal , Humans , Male , Mice , Mice, Inbred BALB C , NF-kappa B/metabolism , Signal Transduction , Trinitrobenzenesulfonic Acid
12.
Med Sci Monit ; 23: 3209-3216, 2017 Jul 01.
Article in English | MEDLINE | ID: mdl-28667247

ABSTRACT

BACKGROUND Mesenchymal stem cells (MSCs) have emerged as an attractive alternative to modulating immune response after transplantation. Recent studies have shown that systemically administered MSCs enter the inflamed intestine. In the present study, we propose a strategy to improve the efficacy of MSC-based cellular therapy for inflammation using Astragaloside and Baicalein to enhance cell survival, inhibit apoptosis, and modulate inflammatory response in vitro. MATERIAL AND METHODS MSCs were induced with lipopolysaccharide (LPS) as an inflammatory model before being treated for 48 h with Astragaloside, Baicalein, and the combination of both. MSCs proliferation was determined using the MTT method. The cell cycle situation was monitored using flow cytometry, and the apoptosis ability of MSCs was detected with Annexin-V flow cytometry. The levels of cytokine IL-1ß, IL-8, and TNF-α, and their relations with the ERK pathway were measured using ELISA, RT-PCR, and Western blot. RESULTS Compared to the control groups (containing no drug), each drug-treated group showed the ability to promote epithelial differentiation and cell growth and to inhibit apoptosis. The combination group had reduced levels of IL-1ß, IL-8, and TNF-α in LPS-induced MSCs, much more than in the other 2 groups. Compared with the other groups, the combination of Astragaloside and Baicalin more efficiently reduced IL-1ß, IL-8, and TNF-α levels in the LPS-induced MSCs model, and ERK inhibitor was capable of recovering the inflammatory effect. CONCLUSIONS The results demonstrated that Astragaloside and Baicalin can promote epithelial differentiation and proliferation, inhibit apoptosis, and reduce inflammatory effects.


Subject(s)
Extracellular Signal-Regulated MAP Kinases/metabolism , Flavanones/therapeutic use , Inflammation/drug therapy , Inflammation/enzymology , MAP Kinase Signaling System/drug effects , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells/pathology , Saponins/therapeutic use , Animals , Apoptosis/drug effects , Cell Differentiation/drug effects , Cell Proliferation/drug effects , Cell Separation , Cytokines/metabolism , Flavanones/pharmacology , Inflammation/pathology , Male , Mesenchymal Stem Cells/drug effects , Mesenchymal Stem Cells/enzymology , Rats, Sprague-Dawley
13.
Int Immunopharmacol ; 50: 152-160, 2017 Sep.
Article in English | MEDLINE | ID: mdl-28666238

ABSTRACT

Paeoniflorin is traditionally used to treat inflammatory disorders. In our laboratory, we have scientifically validated the anti-inflammatory effect of paeoniflorin. In this study, it has been aimed to evaluate in vivo anti-inflammatory effect of paeoniflorin isolated from the dried peeled root of Paeonia lactiflora Pall. It was further intended to find out the probable mechanism of anti-inflammatory effect of paeoniflorin. The anti-inflammatory effect of paeoniflorin (15, 30 and 45mg/kg) was measured employing TNBS-induced ulcerative colitis model of acute inflammation. The TNBS injection resulted significant colitis formation when compared with un-injected mice. The anti-inflammatory effects of paeoniflorin for ulcerative colitis were assessed by body weight, colonic weight and length, macroscopic scores, and histopathological examinations. In addition, the colonic tissue levels of inflammation markers, including myeloperoxidase (MPO), IL-2, IL-6, IL-10, IL-12, IL-1ß, TNF-α and IFN-γ were also determined to assess the effect of paeoniflorin. In addition, western blot demonstrated that paeoniflorin inhibited NF-kappaB signaling pathway and apoptosis in TNBS-induced ulcerative colitis tissues. In conclusion, all the findings of this study suggested that paeoniflorin has the anti-inflammatory effect in ulcerative colitis via inhibiting MAPK/NF-kappaB pathway and apoptosis in mice.


Subject(s)
Anti-Inflammatory Agents/therapeutic use , Colitis, Ulcerative/drug therapy , Colon/immunology , Glucosides/therapeutic use , Inflammation/drug therapy , Monoterpenes/therapeutic use , Animals , Apoptosis , Colitis, Ulcerative/chemically induced , Colon/drug effects , Colon/pathology , Cytokines/metabolism , Extracellular Signal-Regulated MAP Kinases/metabolism , Humans , Inflammation/chemically induced , Male , Mice , Mice, Inbred BALB C , NF-kappa B/metabolism , Paeonia/immunology , Signal Transduction , Trinitrobenzenesulfonic Acid/toxicity
14.
Zhongguo Zhong Xi Yi Jie He Za Zhi ; 36(2): 191-5, 2016 Feb.
Article in Chinese | MEDLINE | ID: mdl-27078996

ABSTRACT

OBJECTIVE: To observe the effect of Jianpi Bushen Qingchang Huashi Recipe (JBQHR) on proliferation and migration of bone marrow mesenchymal stem cells (BMSCs). METHODS: BMSCs were isolated and cultured in vitro with adherence screening method to prepare cell suspension. No drug intervention was given to BMSCs in the vehicle control group. JBQHR at 0.39, 0.78, 1.56 µg/mL was added in BMSCs of low, mid, and high dose JBQHR groups for co-incubation. Its effect on the proliferation of BMSCs was detected by CCK-8. BMSCs migration and chemotactic ability was detected using Transwell method. Each dose JBQHR combined ERK kinase inhibitor U0126 was set up as control. The phosphorylation of extracellular regulated protein kinase (ERK) and CAMP responsive element-binding protein (CREB) were detected by Western blot. RESULTS: Compared with the vehicle control group, the proliferation of BMSCs and BMSCs migration number could be promoted in the 3 JBQHR groups (P < 0.05). Besides, the proliferation of BMSCs was better in mid and high dose JBQHR groups than in the low dose JBQHR group (P < 0.05). Compared with the vehicle control group, the phosphorylation of ERK and CREB could be elevated in the 3 JBQHR groups (P < 0.05), and could be inhibited by U0126 (P < 0.01). Compared with the low dose JBQHR group, the phosphorylation of ERK increased in mid and high dose JBQHR groups with statistical difference (P < 0.05). CONCLUSION: JBQHR could promote the proliferation and migration of BMSCs, and its mechanism might be related to ERK/CREB signaling pathway


Subject(s)
Drugs, Chinese Herbal/pharmacology , Mesenchymal Stem Cells/drug effects , Cell Movement/drug effects , Cell Proliferation/drug effects , Cells, Cultured , Cyclic AMP Response Element-Binding Protein/metabolism , Extracellular Signal-Regulated MAP Kinases/metabolism , Humans , MAP Kinase Signaling System , Mesenchymal Stem Cells/cytology
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