PMID: 

Biosci Trends. 2020 Feb 9. Epub 2020 Feb 9. PMID: 32037389

Abstract Title: 

Clinical characteristics and therapeutic procedure for four cases with 2019 novel coronavirus pneumonia receiving combined Chinese and Western medicine treatment.

Abstract: 

Pneumonia associated with the 2019 novel coronavirus (2019-nCoV) is continuously and rapidly circulating at present. No effective antiviral treatment has been verified thus far. We report here the clinical characteristics and therapeutic procedure for four patients with mild or severe 2019-nCoV pneumonia admitted to Shanghai Public Health Clinical Center. All the patients were given antiviral treatment including lopinavir/ritonavir (Kaletra), arbidol, and Shufeng Jiedu Capsule (SFJDC, a traditional Chinese medicine) and other necessary support care. After treatment, three patients gained significant improvement in pneumonia associated symptoms, two of whom were confirmed 2019-nCoV negative and discharged, and one of whom was virus negative at the first test. The remaining patient with severe pneumonia had shown signs of improvement by the cutoff date for data collection. Results obtained in the current study may provide clues for treatment of 2019-nCoV pneumonia. The efficacy of antiviral treatment including lopinavir/ritonavir, arbidol, and SFJDC warrants further verification in future study.

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PMID: 

Arch Toxicol. 2020 Jan ;94(1):257-271. Epub 2019 Nov 25. PMID: 31768571

Abstract Title: 

Doxorubicin persistently rewires cardiac circadian homeostasis in mice.

Abstract: 

Circadian rhythms disruption can be the cause of chronic diseases. External cues, including therapeutic drugs, have been shown to modulate peripheral-circadian clocks. Since anthracycline cardiotoxicity is associated with loss of mitochondrial function and metabolic remodeling, we investigated whether the energetic failure induced by sub-chronic doxorubicin (DOX) treatment in juvenile mice was associated with persistent disruption of circadian regulators. Juvenile C57BL/6J male mice were subjected to a sub-chronic DOX treatment (4 weekly injections of 5 mg/kg DOX) and several cardiac parameters, as well as circadian-gene expression and acetylation patterns, were analyzed after 6 weeks of recovery time. Complementary experiments were performed with Mouse Embryonic Fibroblasts (MEFs) and Human Embryonic Kidney 293 cells. DOX-treated juvenile miceshowed cardiotoxicity markers and persistent alterations of transcriptional- and signaling cardiac circadian homeostasis. The results showed a delayed influence of DOX on gene expression, accompanied by changes in SIRT1-mediated cyclic deacetylation. The mechanism behind DOX interference with the circadian clock was further studied in vitro, in which were observed alterations of circadian-gene expression and increased BMAL1 SIRT1-mediated deacetylation. In conclusion, DOX treatment in juvenile mice resulted in disruption of oscillatory molecular mechanisms including gene expression and acetylation profiles.

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PMID: 

Front Oncol. 2019 ;9:1431. Epub 2020 Jan 9. PMID: 31998631

Abstract Title: 

Glycyrrhizic Acid-Induced Differentiation Repressed Stemness in Hepatocellular Carcinoma by Targeting c-Jun N-Terminal Kinase 1.

Abstract: 

Hepatocellular carcinoma (HCC) is one of the most common malignant cancers with poor prognosis and high incidence. Cancer stem cells play a vital role in tumor initiation and malignancy. The degree of differentiation of HCC is closely related to its stemness. Glycyrrhizic acid (GA) plays a critical role in inhibiting the degree of malignancy of HCC. At present, the effect of GA on the differentiation and stemness of HCC has not been reported, and its pharmacological mechanism remains to be elucidated. This study evaluated the effect of GA on the stemness of HCC and investigated its targets through proteomics and chemical biology. Results showed that GA can repress stemness and induce differentiation in HCC. GEO analysis revealed that cell differentiation and stem cell pluripotency were up-regulated and down-regulated after GA administration, respectively. Virtual screening was used to predict the c-Jun N-terminal kinase 1 (JNK1) as a direct target of GA. Moreover, chemical biology was used to verify the interaction of JNK1 and GA. Experimental data further indicated that JNK1 inhibits stemness and induces differentiation of HCC. GA exerts its function by targeting JNK1. Clinical data analysis from The Cancer Genome Atlas also revealed that JNK1 can aggravate the degree of malignancy of HCC. The results indicated that, by targeting JNK1, GA can inhibit tumor growth through inducing differentiation and repressing stemness. Furthermore, GA enhanced the anti-tumor effects of sorafenib in HCC treatment. These results broadened our insight into the pharmacological mechanism of GA and the importance of JNK1 as a therapeutic target for HCC treatment.

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PMID: 

Iran J Pharm Res. 2018 ;17(2):726-734. PMID: 29881429

Abstract Title: 

Chemical Profile and Anti-inflammatory Activity of Total Flavonoids fromFisch.

Abstract: 

Fisch. () is one of the most widely used herbal medicines. This study was designed to enrich total flavonoids (TFF) from. The chemical profile of TFF was identified by HPLC and colorimetric assay. The TFF mainly contained liquiritin apioside, liquiritin, isoliquiritin apioside, liquiritigenin and isoliquiritigenin without glycyrrhizic acid. To study the anti-inflammatory activity of TFF, the DMB-induced ear vasodilatation assay and carrageenan-induced rat paw edema model have been utilized. Treatment with TFF showed significant anti-inflammatory activities in the two models. The twoedema assays demonstrated that the TFF possesses significant dose-dependent anti-inflammatory activity, similar to that of indomethacin at a dose of 500 mg/kg. In rat paws with carrageenan, treatment with TFF (500 and 250 mg/kg) markedly inhibited the expression of IL-1β and iNOS. TFF at all doses noticeably decreased levels of NO and MDA at the site of inflammation, while only i.g. TFF at a dose of 500 mg/kg significantly decreased TNF-α levels in the carrageenan-injected paws. In addition, an increase in SOD activity was induced by TFF at all doses. These results revealed that TFF exhibited significant anti-inflammatory activity in acute inflammatory models.

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PMID: 

J Pharmacol Sci. 2018 Aug ;137(4):324-332. Epub 2018 May 5. PMID: 30150145

Abstract Title: 

Inhibition effect of glycyrrhiza polysaccharide (GCP) on tumor growth through regulation of the gut microbiota composition.

Abstract: 

Glycyrrhiza Uralensis Polysaccharide (GCP), as a macromolecular polysaccharide extracted from the Traditional Chinese Medicine (TCM) – Licorice has been proved to inhibit tumor growth in vitro and in vivo; however, the specific anti-tumor mechanism of GCP needs to be further investigated. In this study, we explore the anti-tumor mechanism of GCP from the angle of gut microbiota. Colon carcinoma cells (CT-26) were used to set up a tumor-bearing mouse model. After 14 days of GCP treatment, the weights of tumors were significantly reduced. In addition, HE staining of tissue sections reflected that GCP could effectively inhibit tumor metastasis. 16SrRNA high-throughput sequencing of fecal samples showed a significant change between the model group and GCP group in the composition of gut microbiota. Subsequently, gut microbiota depletion and fecal transplantation experiments further confirmed the relationship between the anti-tumor effects of GCP and gut microbiota. Following depletion of gut microbiota, GCP cannot inhibit tumor growth. Fecal transplantation experiments found that transplanting the feces of GCP-treated mice, to a certain extent, could inhibit tumor growth and metastasis. These results indicate that Glycyrrhiza Polysaccharides exert anti-tumor effects by affecting gut microbiota composition.

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PMID: 

Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2019 Oct 20 ;37(10):737-745. PMID: 31726503

Abstract Title: 

[Antioxidant mechanism of diallyl sulfide in inhibiting leucopenia in peripheral blood induced by benzene in rats].

Abstract: 

To investigate the antioxidant mechanism of diallyl sulfide (DAS) in antagonizing the reduction in peripheral blood white blood cells (WBC) induced by benzene in rats.A total of 60 specific pathogen-free adult male Sprague-Dawley rats, with a body weight of 180-220 g, were selected, and after 5 days of adaptive feeding, they were randomly divided into blank control group, DAS control group, benzene model group, benzene+low-dose DAS group, benzene+middle-dose DAS group, and benzene+high-dose DAS group, with 10 rats in each group. The rats in the benzene+low-dose DAS group, the benzene+middle-dose DAS group, the benzene+high-dose DAS group, and the DAS control group were given DAS by gavage at a dose of 40, 80, 160, and 160 mg/kg·bw, respectively, and those in the blank control group and the benzene model group were given an equal volume of corn oil; 2 hours later, the rats in the benzene model group, the benzene+low-dose DAS group, the benzene+middle-dose DAS group, and the benzene+high-dose DAS group were given a mixtureof benzene (1.3 g/kg·bw) and corn oil (with a volume fraction of 50%), and those in the blank control group and the DAS control group were given an equal volume of corn oil. The above treatment was given once a day for 4 consecutive weeks. At 1 day before treatment, anticoagulated blood was collected from the jugular vein for peripheral blood cell counting. After anesthesia with intraperitoneally injected pentobarbital (50 mg/kg·bw), blood samples were collected from the abdominal aorta, serum was isolated, and the thymus, the spleen, and the femur were freed at a low temperature to measureoxidative and antioxidant indices. The femur at one side was freed for WBC counting in bone marrow.Compared with the blank control group, the benzene model group had significant reductions in the volume, weight, and organ coefficient of the spleen and the thymus (

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PMID: 

Toxicol Mech Methods. 2020 Mar ;30(3):208-218. Epub 2019 Dec 9. PMID: 31779506

Abstract Title: 

Diallyl sulfide alleviates cyclophosphamide-induced nephropathic encephalopathy in rats.

Abstract: 

Diallyl sulfide (DAS) is a garlic-derived organosulfur compound. The current study was planned to evaluate the protecting effects of DAS against cyclophosphamide (CP)-induced nephropathic encephalopathy. DAS (100 mg/kg) was orally administered for 4 days, 60 min after the last dose, rats were injected with CP (150 mg/kg). DAS treatment before CP significantly decreased serum urea, creatinine, sodium, potassium, calcium, blood urea nitrogen (BUN), C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-1β (IL-1ß) and tumor necrosis factor-alpha (TNF-α) compared with CP-treated rats. DAS treatment decreased malondialdehyde (MDA) and increased superoxide dismutase (SOD) and reduced glutathione (GSH) levels in the renal tissues and significantly attenuated the elevated neurotransmitters N-methyl-D-aspartate/adenosine triphosphate (NMDA), γ-aminobutyric acid (GABA) levels and remarkably restored neuronal nitric oxide (NO) level and nitric oxide synthase (nNOS) activity in the brain compared to CP-treated rats. DAS for 4 consecutive days before CP showed moderate positive immunohistochemically expression of the glial fibrillary acidic protein (GFAP) in the brain and kidney tissues comparable to CP-treated rats. DAS afforded renal and neuroprotection against CP-induced nephropathic encephalopathy due to its capacity to ameliorates the afore-mentioned biochemical parameters which were supported by histopathological and immunohistochemically examination.

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PMID: 

Exp Ther Med. 2020 Feb ;19(2):1507-1510. Epub 2019 Dec 27. PMID: 32010331

Abstract Title: 

The preventive and therapeutic application of garlic and other plant ingredients in the treatment of periodontal diseases.

Abstract: 

Since ancient times, pharmacologically active ingredients derived from natural sources, including plants and microbials have been used in the treatment of a wide array of diseases, such as atherosclerosis, diabetes mellitus and cancers. Herbal extracts and polyphenols are produced from herbs that contain a variety of ingredients, most of which exhibit anti-inflammatory, anti-oxidative and anti-microbial actions. Gingivitis is triggered by the infection of the periodontal tissues with periodontal disease-causing pathogens present in the dental biofilm. This is accompanied by weak inflammatory immune reactions in the gingiva. In periodontitis, prolonged and excessive inflammation results in the destruction of gingival connective tissue and in the resorption of alveolar bone, leading to tooth loss. There are a number of clinical reports showing the effectiveness of both herbal extracts and polyphenols on periodontal diseases when applied as a mouthwash or dentifrice into the oral cavity. However, to date, at least to the best of our knowledge, there is no clinical report available on the therapeutic effects of garlic or its extract on periodontal diseases, apart from a recent study, which reported that the intake of aged garlic extract (AGE) containing various pharmacologically active sulfur compounds, alleviated the symptoms of gingivitis clinically. The finding suggests that AGE may be a promising candidate for use in the treatment of periodontal diseases, although additional clinical trials are warranted to confirm this. In addition, further studies are required for the clarification of the basic molecular mechanisms through which AGE attenuates gingivitis. In this review, we summarize the beneficial effects of several natural compounds on periodontal disease and describe the possible applications of garlic ingredients in detail.

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PMID: 

Oncol Lett. 2018 Jan ;15(1):623-629. Epub 2017 Oct 26. PMID: 29285203

Abstract Title: 

Anticancer effect of S-allyl-L-cysteine via induction of apoptosis in human bladder cancer cells.

Abstract: 

To examine the anticancer effects of S-allyl-L-cysteine (SAC) in human bladder cancer cells and to identify possible molecular mechanisms, bladder cancer cell lines (HTB5, HTB9, JON, UMUC14, T24, and cisplatin resistant-T24R2) were incubated with SAC, and cell proliferation was measured using the Cell Counting Kit-8 assay and clonogenic assay. Cell cycle and apoptosis were evaluated by flow cytometry. Expression levels of apoptosis- and cell cycle-associated proteins were analyzed by western blotting. Proliferation and colony formation in bladder cancer cells was significantly inhibited by SAC treatment in a dose-dependent manner. SAC treatment significantly enhanced apoptosis and promoted a cell cycle arrest in the S phase. SAC also increased the expression of apoptosis-related genes, including caspases, poly (ADP-ribose) polymerase and cytochrome c. SAC had an anticancer effect on bladder cancer cells, at least partially, through the induction of apoptosis and a cell cycle arrest. SAC is a potential therapeutic agent for the treatment of bladder cancer.

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PMID: 

J Pharmacol Sci. 2019 Apr ;139(4):377-384. Epub 2019 Mar 14. PMID: 30928090

Abstract Title: 

S-allyl-l-cysteine attenuates bleomycin-induced pulmonary fibrosis and inflammation via AKT/NF-κB signaling pathway in mice.

Abstract: 

Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by inflammation, multifocal fibrotic lesions and excessive collagen deposition with limited therapies. As a major bioactive compound in garlic, S-allyl-l-cysteine (SAC) is a neuroprotective drug candidate to prevent cognitive decline, however, its anti-pulmonary fibrotic activity remains unknown. Here, we investigated whether SAC could attenuate bleomycin (BLM)-induced pulmonary fibrosis and inflammation in mice. Our results showed that SAC dose-dependently reduced the infiltration of inflammatory cells, pulmonary lesions and collagen deposition in BLM treated mice with downregulated mRNA expression levels of fibrotic genes including alpha smooth muscle actin (α-SMA), fibronectin, collagen I and collagen III as well as the protein level of α-SMA. In addition, SAC could also reduce the mRNA expression of inflammatory mediators such as TNF-α and iNOS. Furthermore, higher phosphorylation of AKT and NF-κB p65 in IPF patient samples and murine samples wasverified by immunohistochemistry while SAC could decrease the phosphorylation level of AKT and NF-κB p65 in mice stimulated with BLM. These findings, for the first time, indicate that SAC might mediate AKT/NF-κB signaling pathway to inhibit BLM-induced pulmonary fibrosis and support the potentialrole of SAC as an anti-pulmonary fibrosis agent.

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