1.Q-marker analysis of Kanggongyan soft capsule
Minyan YUAN ; Min ZHANG ; Shuo ZHANG ; Siyuan CAO ; Jiacheng JI ; Pengjiao WANG ; Rongping ZHANG ; Xiuli GAO
China Pharmacy 2022;33(17):2082-2086
OBJECTIVE To analyze quality maker (Q-marker) of Ka nggongyan soft capsule (KSC). METHODS The fingerprints of 20 batches of KSC were established by ultra high performance liquid chromatography (UPLC)method. Similarity Evaluation System of TCM Chromatographic Fingerprint (2012 edition)were used to evaluate the similarity and confirm common peaks. The contents of norisoboldine ,leonurine hydrochloride ,forsythoside B ,acteoside,poliumoside and isoacteoside were determined by the same UPLC method. Targets and pathways related to KSC in the treatment of cervicitis were screened and analyzed by network pharmacology and molecular docking method to construct a “component-target-pathway”network,and analyze its potential Q-marker. RESULTS Twelve common peaks were identified in the fingerprints of 20 batches of KSC ,and the similarity was greater than 0.99. Six common peaks were identified ,including norisoboldine ,leonurine hydrochloride ,forsythoside B,acteoside,poliumoside and isoacteoside. The contents of the above 6 components were 1.336-1.774,0.093-0.143,4.970-5.888, 0.505-0.623,5.206-6.226 and 0.785-0.895 mg/g,respectively. By network pharmacology analysis ,14 key targets and 94 pathways were obtained ,and their binding energies to the core targets (protein kinase B 1,tumor necrosis factor )were all less than -6.4 kJ/cal. CONCLUSIONS Six components such as norisoboldine and leonurine hydrochloride are potential Q-marker of KSC.
2.Improvement effect and mechanism of Baicao fuyanqing suppository on bacterial vaginitis in rats
Qi WANG ; Pengjiao WANG ; Xiaodong SUN ; Min ZHANG ; Minyan YUAN ; Xiaoxia MENG ; Yanni ZHAO ; Shuo ZHANG ; Xiuli GAO
China Pharmacy 2023;34(20):2476-2482
OBJECTIVE To explore the improvement effect and potential mechanism of Baicao fuyanqing suppository on bacterial vaginitis (BV) in rats. METHODS The female SD rats were randomly divided into normal group, model group, metronidazole group (positive control, 0.03 g/kg), Baicao fuyanqing suppository low-dose, medium-dose and high-dose groups (0.18, 0.36, 0.72 g/kg), with 8 rats in each group. Except for the normal group, the rats in other groups were injected subcutaneously with 0.2 g of Estradiol benzoate injection+20 μL of Escherichia coli suspension (2×108~3×108 cfu/mL) through the vaginal opening to establish the BV rat model. Administration groups were given relevant medicine vaginally, while the normal group and the model group were given normal saline, once a day, for 6 consecutive days. Twenty-four hours after the last administration, the vaginal appearance score and vaginal pH were measured for each group of rats. The levels of cytokines [interleukin-1β (IL-1β), IL-2, IL-13, immunoglobulin A (IgA)] in vaginal lavage fluid were determined. The morphology of the uterus and accessories, and pathological changes in the vaginal tissue were observed. The expressions of Toll-like receptor 2 (TLR2), TLR4 and nuclear factor-κB (NF-κB) in vaginal tissues were determined. RESULTS Compared with the normal group, the uterus edema, the irregular shape of uterus and accessories, the vaginal mucosa hyperplasia, and the massive desquamation of epithelial cells were observed in the model group, complicating with massive infiltration of inflammatory cells; vaginal opening redness and swelling score and secretion score, vaginal pH, the levels of proinflammatory cytokine IL-1β and IL-2, the protein expressions of TLR2, TLR4 and NF- κB were all increased or up-regulated, while the levels of IgA and anti-inflammatory cytokine IL-13 decreased significantly (P<0.05 or P<0.01). Compared with the model group, varying cn degrees of improvement in uterine and accessories, and vaginal tissue lesions in rats were observed in administration groups, and most of the quantitative indicators mentioned above showed significant improvement (P<0.05 or P<0.01). CONCLUSIONS Baicao fuyanqing suppository has a certain improvement effect on inflammatory symptoms in BV rats, and its mechanism may be related to the inhibition of the TLR/NF-κB signaling pathway.
3.Targeted inhibition of osteoclastogenesis reveals the pathogenesis and therapeutics of bone loss under sympathetic neurostress.
Bingdong SUI ; Jin LIU ; Chenxi ZHENG ; Lei DANG ; Ji CHEN ; Yuan CAO ; Kaichao ZHANG ; Lu LIU ; Minyan DANG ; Liqiang ZHANG ; Nan CHEN ; Tao HE ; Kun XUAN ; Fang JIN ; Ge ZHANG ; Yan JIN ; Chenghu HU
International Journal of Oral Science 2022;14(1):39-39
Sympathetic cues via the adrenergic signaling critically regulate bone homeostasis and contribute to neurostress-induced bone loss, but the mechanisms and therapeutics remain incompletely elucidated. Here, we reveal an osteoclastogenesis-centered functionally important osteopenic pathogenesis under sympatho-adrenergic activation with characterized microRNA response and efficient therapeutics. We discovered that osteoclastic miR-21 was tightly regulated by sympatho-adrenergic cues downstream the β2-adrenergic receptor (β2AR) signaling, critically modulated osteoclastogenesis in vivo by inhibiting programmed cell death 4 (Pdcd4), and mediated detrimental effects of both isoproterenol (ISO) and chronic variable stress (CVS) on bone. Intriguingly, without affecting osteoblastic bone formation, bone protection against ISO and CVS was sufficiently achieved by a (D-Asp8)-lipid nanoparticle-mediated targeted inhibition of osteoclastic miR-21 or by clinically relevant drugs to suppress osteoclastogenesis. Collectively, these results unravel a previously underdetermined molecular and functional paradigm that osteoclastogenesis crucially contributes to sympatho-adrenergic regulation of bone and establish multiple targeted therapeutic strategies to counteract osteopenias under stresses.
Adrenergic Agents/pharmacology*
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Apoptosis Regulatory Proteins/pharmacology*
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Bone Diseases, Metabolic/metabolism*
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Humans
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Liposomes
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MicroRNAs/genetics*
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Nanoparticles
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Osteoclasts
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Osteogenesis/physiology*
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RNA-Binding Proteins/pharmacology*