Spices have enjoyed a long history and a worldwide application. Of particular interest is the pharmaceutical value of spices in addition to its basic seasoning function in cooking. Concretely, equipped with complex chemical compositions, spices are of significant importance in pharmacologic actions, like antioxidant, antibacterial, antitumor, as well as therapeutical effects in gastrointestinal disorders and cardiovascular disease. Although increasing evidences in support of its distinct role in the medical field has recently reported, little information is available for substantive, thorough and sophisticated researches on its chemical constituents and pharmacological activities, especially mechanism of these actions. Therefore, in popular wave of studies directed at a single spice, this review presents systematic studies on the chemical constituents and pharmacological activities associated with common used spices, together with current typical individual studies on functional mechanism, in order to pave the way for the exploitation and development of new medicines derived from the chemical compounds of spice (such as, piperine, curcumin, geniposide, cinnamaldehyde, cinnamic acid, linalool, estragole, perillaldehyde, syringic acid, crocin).
Anti-Infective Agents ; pharmacology ; Antineoplastic Agents ; pharmacology ; Antioxidants ; pharmacology ; Cardiovascular System ; drug effects ; Digestive System ; drug effects ; Spices ; analysis ; toxicity

Objective To investigate the effects of transient receptor potential vanilloid 1 activation by capsaicin on the oxidative stress in lipopolysaccharide-induced lung injury in mice in order to elucidate the potential mechanisms.Methods A total of 108 specific pathogen free (SPF) ICR male mice were randomly divided into six groups:normal control group (n =18),capsaicin control group (CAP control group,n =18),capsazepine control group (CAPZ control group,n =18),acute lung injury group (n =18),capsaicin treatment group (CAP treatment group,n =18) and capsazepine treatment group (CAPZ treatment group,n =18).After modeling,superoxide dismutase (SOD),catalase (CAT) and malondiachehyche (MDA) levels in lung were measured with the method of chromatometry,and the expression of heme oxygenase 1 (HO-1) in lung tissue was assessed with enzyme linked immunosorbent assay (ELISA),while the level of NF-E2-related factor-2 (Nrf2) was determined by western blotting and the expression of Nrf2 mRNA was measured by RTPCR.Pathological changes of lung tissue were observed under light microscope.Results The activities of SOD and CAT in lung tissue at 3,8,16 h were dramatically lower in acute lung injury group than those in normal control group (P ＜ 0.05),while the level of MDA was higher.Compared with acute lung injury group,the lung levels of SOD and CAT at 8 h and 16 h were higher in CAP treatment group (P ＜0.05),while the lung level of MDA was lower (P ＜ 0.05).The levels of SOD and CAT in CAPZ treatment group were decreased at 8 h and 16 h,while the levels of MDA in this group were increased at 3,8,16 h (P ＜0.05).The pulmonary levels of HO-1,Nrf2 and expression of Nrf2 mRNA were significantly higher in acute lung injury group than those in normal control group (P ＜ 0.05).Compared with acute lung injury group,the levels of HO-1,NRF2 and expression of NRF2 mRNA were increased markedly in CAP treatment group (P ＜ 0.05)and were obviously decreased in CAPZ treatment group (P ＜0.05).At 8 h,16 h after modeling,the degree of lung damage was ameliorated in CAP treatment group compared with acute lung injury group under light microscope,while the lung damage was aggravated in CAPZ treatment group.Conclusions The activation of TRPV1 could apparently up-regulate the levels of CAT,SOD,Nrf2,HO-1,and reduce the MDA level in lung tissue of mice with acute lung injury,ultimately protecting the endotoxemia mice from oxidative stress.

Female ; Humans ; Infant, Newborn ; Mastocytosis, Systemic ; diagnosis ; pathology

Background and purpose: Sorafenib hepatocellular carcinoma assessment randomized protocol (SHARP) and sorafenib in patients in Asia-Pacific region with hepatocellular carcinoma (ORIENTAL) had indicated that multi-kinase inhibitor sorafenib could prolong overall survival (OS) and time to progression (TTP) as well as improve progress free survival (PFS) in patients with advanced stage hepatocellular carcinoma. Drug-related adverse events in the course of treatment restricted its clinical application to a certain degree. This study was aimed to summerize the adverse events as well as the management of sorafenib in our clinic. Methods: Twenty-five cases clinically diagnosed as advanced hepatocellular carcinoma were enrolled from January 2008 to October 2009. All the patients who received sorafenib treatment met inclusion criteria as followed: (1) Progression of disease after trans-hepatic arterial chemoembolization therapy; (2) Extensive portal vein cancerous thrombus formation; (3) Portal zone or retroperitoneal lymph node metastasis or multiple remote metastasis, such as lung or bone; (4) Diffused poor blood supply to tumor; (5) Inform consent was obtained. All adverse events with different grade were observed during the beginning 12 weeks, and clinical treatment were carried out relatively. Results: Total of 25 cases were enrolled. Nine patients died of the disease, 3 of them died during the first 12 weeks, 3 patients abandoned sorafenib treatment, among them 2 died before the finish of 12 weeks treatment and 1 patient discontinued 5 months after the sorafenib treatment. Twenty cases finally assigned. Number of patients encountered drug-related adverse events were: HFSR (hand-foot-skin-reaction) 4(4/20), diarrhea 4(4/20), alopecia 5(5/20), rasb 4(4/20), fatigue 8(8/20), leukopenia and Thrombocytopenia 4(4/20), elevated blood pressure 1(1/20) and abdominal pain 1(1/20). After clinical management, 20 patients' sorafenib treatment were eventually not affected by adverse events. Conclusion: Sorafenib was well-tolerated and is a safe option of treatment for patients with advanced hepatocellular carcinoma.

Abstracting and Indexing as Topic ; Neoplasms ; Periodicals as Topic

OBJECTIVETo investigate the intervention effect of thalidomide on paraquat-induced acute lung injury in mice and its mechanism.

METHODSMale ICR mice were randomly allocated to negative control group (n = 30), thalidomide control group (n = 30), paraquat poisoning group (n = 30), 50 mg/kg thalidomide treatment group (n = 30), 100 mg/kg thalidomide treatment group (n = 30), and 150 mg/kg thalidomide treatment group (n = 30). The negative control group was intraperitoneally injected with the same volume of saline; the thalidomide control group was intraperitoneally injected with thalidomide (150 mg/kg); the paraquat poisoning group was intraperitoneally injected with diluted paraquat solution (22 mg/kg); each thalidomide treatment group was intraperitoneally injected with the same volume of paraquat solution (22 mg/kg) and was injected with thalidomide (50, 100, or 150 mg/kg) 1 h later. All mice were anesthetized and sacrificed at 1, 3, or 7 d after paraquat poisoning, and their lung tissue was collected. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in lung tissue were measured by double-antibody sandwich ELISA; the mRNA expression of nuclear factor-kappa B (NF-κB) was measured by RT-PCR; the protein expression of nuclear NF-kgr;B p65 was measured by Western blot. The pathological changes of lung tissue were observed under light microscope; the wet/dry ratio of the lung was calculated.

RESULTSCompared with the negative control group, the paraquat poisoning group had significantly increased levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65 and wet/dry ratio of the lung (P < 0.05). Compared with the paraquat poisoning group, the thalidomide treatment groups had significantly decreased levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65 and wet/dry ratios of the lung (P < 0.05), and the 150 mg/kg thalidomide treatment group showed the most significant decrease in the levels of TNF-α, IL-1β, IL-6, NF-κB mRNA, and nuclear NF-κB p65. The observation of pathological changes showed that the paraquat poisoning group had the most marked lung tissue damage at 3 d after poisoning, and the lung tissue damage was lessened in the thalidomide treatment groups.

CONCLUSIONThalidomide can reduce paraquat-induced acute lung injury and lung edema. The mechanism may include inhibition of NF-κB activation and expression and downregulation of TNF-α, IL-1β, and IL-6.

Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Cytokines ; metabolism ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred ICR ; NF-kappa B p50 Subunit ; metabolism ; Paraquat ; poisoning ; Thalidomide ; pharmacology ; Transcription Factor RelA ; metabolism

OBJECTIVETo investigate the effect of Compound Qingqin Liquid (CQL) on the expression level of angiotensin II (Ang II) and COX-2 mRNA transcription and protein expression in the renal tissue of rats with uric acid nephropathy.

METHODSSD rats were randomly divided into the blank control group, the model group, the positive drug group, the high, moderate, and low dose CQL group according to number randomization principle. The model was established by gastrogavage of adenine, accompanied with yeast feeding. Distilled water was given by gastrogavage to rats in the blank control group and the model group. Allopurinol at the daily dose of 9.33 mg/kg was given by gastrogavage to rats of the positive control group. CQL at the daily dose of 3.77 g/kg, 1.89 g/kg, and 0.09 g/kg was respectively given by gastrogavage to rats in the high, moderate, and low dose CQL groups. All treatment lasted for 6 weeks. Rats were randomly divided at week 4 (3 in the blank control group, and 6 in the rest groups), and the rest rats were killed at week 6. The renal tissue was extracted. The expression level of Ang II and COX-2 mRNA transcription were detected by RT-PCR. The expression level of Ang II was detected by ELISA. The expression level of COX-2 protein was detected by Western blot and immunohistochemical assay.

RESULTSCompared with the blank control group, except the mRNA expression of Ang II at week 4, the mRNA and protein expression of Ang II and COX-2 obviously increased at week 4 and 6 in the model group (P < 0.01, P < 0.05). The COX-2 protein expression at week 4 was obviously lower in the high and moderate dose CQL groups than in the model group and the low dose CQL group (P < 0.05); the average integral of optical density value was obviously lower in the positive control group than in the model group. Except the mRNA expression of Ang II in the high dose CQL group at week 6, the mRNA and protein expression of Ang II obviously decreased in the positive control group and each dose CQL group (P < 0.01, P < 0.05). Of them, the effects were better in the high and moderate dose CQL groups than in the positive control group and the low dose CQL group (P < 0.05, P < 0.01). Besides, the mRNA expression of COX-2, the average integral of optical density value were obviously lower in the positive control group and each dose CQL group than in the model group (P < 0.05). The protein expression of COX-2 was obviously lower in the high and moderate dose CQL groups than in the model group (P < 0.05). Of them, the mRNA expression of COX-2 was better in the moderate dose CQL group than in the positive control group (P < 0.05); the protein expression of COX-2 was better in the high dose CQL group than in the low dose CQL group (P < 0.05).

CONCLUSIONCQL was capable of lowering the expression level of Ang II, COX-2 mRNA transcription and protein expression, thus suppressing the inflammatory pathological injury of the renal tissue.

Angiotensin II ; metabolism ; Animals ; Cyclooxygenase 2 ; genetics ; metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; pharmacology ; Kidney ; metabolism ; Kidney Diseases ; drug therapy ; metabolism ; Male ; RNA, Messenger ; genetics ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Uric Acid

BACKGROUND: Exosomes derived from breast cancer have been reported to play a role in promoting cell proliferation, migration, and angiogenesis, which has the potential to accelerate the healing process of diabetic wounds. The aim of this investigation was to examine the function of exosomes originating from 4T1 mouse breast carcinoma cells (TEXs) in the process of diabetic wound healing. METHODS: The assessment of primary mouse skin fibroblasts cell proliferation and migration was conducted through the utilization of CCK-8 and wound healing assays, while the tube formation of HUVECs was evaluated by tube formation assay. High-throughput sequencing, RT-qPCR and cell experiments were used to detect the roles of miR-126a-3p in HUVECs functions in vitro. The in vivo study employed a model of full-thickness excisional wounds in diabetic subjects to explore the potential therapeutic benefits of TEXs. Immunohistochemical and immunofluorescent techniques were utilized to evaluate histological changes in skin tissues. RESULTS: The findings suggested that TEXs facilitate diabetic wound healing through the activation of cell migration, proliferation, and angiogenesis. An upregulation of miR-126a-3p has been observed in TEXs, and it has demonstrated efficient transferability from 4T1 cells to HUVEC cells. The activation of the PI3K/Akt pathway has been attributed to miR-126a-3p derived from TEXs. CONCLUSIONS The promotion of chronic wound healing can be facilitated by TEXs through the activation of cellular migration, proliferation, and angiogenesis. The activation of the PI3K/Akt pathway by miR-126a-3p originating from TEXs has been discovered, indicating a potential avenue for enhancing the regenerative capabilities of wounds treated with TEXs.

OBJECTIVETo investigate the clinical features and prognosis of malignancy-associated hemophagocytic lymphohistiocytosis (MAHS) in children.

METHODSA retrospective analysis was performed for the primary diseases, clinical features, and prognosis of 24 children with MAHS.

RESULTSAmong the 24 children, 11 (46%) had MAHS induced by tumor and 13 (54%) had chemotherapy-associated MAHS. As for primary diseases, 17 children had acute leukemia, 6 had lymphoma, and 1 had neuroblastoma. The most common clinical manifestations were pyrexia, respiratory symptoms, and hepatosplenomegaly. The most common laboratory abnormalities were hemocytopenia, elevated serum ferritin, and elevated lactate dehydrogenase. Of the 24 children, 22 were treated according to the HLH-2004 protocol and 2 gave up treatment; 18 children died, 1 was lost to follow-up, and 5 survived. The survival time ranged from 3 days to 2 years and 4 months (median 28 days).

CONCLUSIONSChildren with MAHS have various clinical features and extremely poor treatment outcomes.

Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Lymphohistiocytosis, Hemophagocytic ; mortality ; therapy ; Male ; Neoplasms ; complications ; Prognosis ; Retrospective Studies ; Treatment Outcome

Instruction is the basis for the clinical use of drugs and is the safe and effective legal basis for patient to protect their use of drugs. However, the dosage and usage of the instruction in the clinical practice can not meet the clinical needs, which lead to the excessive usage.In this paper, expert consensus on the excessive use of antimicrobial agents beyond the instruction is interpreted in order to provide reference for clinical medication.