Baicalin alleviates TNBS-induced colitis by inhibiting PI3K/AKT pathway activation.

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.

[Analysis on acupoint selection rules for reflux esophagitis].

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)".

Qing Chang Hua Shi granule ameliorate inflammation in experimental rats and cell model of ulcerative colitis through MEK/ERK signaling pathway.

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.

Astragalus and Baicalein Regulate Inflammation of Mesenchymal Stem Cells (MSCs) by the Mitogen-Activated Protein Kinase (MAPK)/ERK Pathway.

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.

[Effect of Jianpi Bushen Qingchang Huashi Recipe on Proliferation of Bone Marrow Mesenchymal Stem Cells].

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