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At least 973 records · Page 54Linked to original sources
PubMed1992

An out-break of epidemic dropsy in the Barabanki District of Uttar Pradesh, India: a limited trial for the scope of antioxidants in the management of symptoms.

An attempt was made to explore the scope of the bio-antioxidants in the management of symptoms of epidemic dropsy caused by argemone alkaloids, sanguinarine and dihydrosanguinarine. The study was performed on 24 randomly selected epidemic dropsy cases who consumed argemone contaminated mustard oil. On examination the cases revealed characteristic pitting edema over limbs (95.8%) accompanied by tenderness (79.2%) and diffuse erythema (95.8%). Tachycardia was present in 1/3 of the examined cases while elevated jugular venous pressure was seen in over 40% of the cases. In two of the cases, reddish-purplish blotches over lower limbs, not raised and which blanched on pressure, was an unusual feature. Chest X-ray revealed pulmonary congestion in 5 cases. ECG performed in 3 cases with severe breathlessness, showed non-specific ST-T changes most marked in L2,L3, avF and V2-V6 which reversed on recovery. Treatment with a combination of antioxidants, riboflavin and tocopherol showed improvement in pain in lower limbs (75%), edema (83.3%) and erythema (66.6%).

Adolescent↗
PubMed2003

Signaling via histamine receptors in cat duodenal smooth muscle cells.

Histamine produced concentration-dependent contractions in cat duodenal smooth muscle cells that were obtained by enzymatic digestion of smooth muscle with collagenase F. Pyrilamine, an H1 receptor antagonist, inhibited the contractile response while famotidine, an H2 receptor antagonist, augmented it. In cells with selectively preserved H1 receptors, produced by pretreatment with pyrilamine followed by inactivation of all unprotected receptors with N-ethylmaleimide, histamine-induced contraction was significantly augmented as compared with control cells. Pertussis toxin (PTX) had no effect on contraction, suggesting that the H1 receptor is coupled to a PTX-insensitive G protein. Gi2, Gi3, Go, Gs, and Gq subunits were present in cat duodenum, and histamine-induced contraction was inhibited by Gq antibody after cell permeabilization. Neomycin, a PLC inhibitor, inhibited the histamine-induced cell contraction, but not rhoCMB, a PLD inhibitor, or DEDA, a PLA2 inhibitor. Heparin, an IP3 receptor inhibitor, inhibited contraction whereas chelerythrine, a PKC inhibitor, had no effect. We conclude that histamine-induced contraction in cat duodenal smooth muscle cells is mediated by H1 receptors coupled to a PTX-insensitive Gq protein and results in activation of phosphatidylinositol-specific phospholipase C (PI-PLC).

Alkaloids↗
PubMed2003

Modulation of CD40L antigen expression in Jurkat cells: involvement of protein kinase C activity.

The CD40L expressed on activated CD4+ T cells delivers contact-dependent proliferative and anti-apoptotic signals to B lymphocytes. Little is known about molecular mechanisms of constitutive expression of CD40L on some non-Hodgkin's lymphomas, especially about involvement of two signal pathways regulating its expression in normal cells; one involving calcineurin, and the other protein kinase C. We analyzed by flow cytometry the effects of 6-hour stimulation of both pathways (stimuli: PMA and ionomycin) and their inhibitors: cyclosporin A and chelerythrine, on CD40L expression. Two Jurkat clones differing in CD40L surface expression: clone 217.6 (CD40L-) and 217.7 (CD40L+) were studied. Our experiments showed that high level of CD40L expression on the surface of 217.7 cells was reduced after stimulation with PMA. The same effect was observed for combination of PMA and chelerythrine or for PKC inhibitor alone. In 217.6 cells, only chelerythrine used alone induced low level of CD40L expression, while PMA and ionomycin were without effect. These results suggest that CD40L surface expression is mainly dependent on protein kinase C activity. By using PepTag Assay we have confirmed that in both Jurkat clones PKC activity is higher than in normal blood lymphocytes.

Alkaloids↗
PubMed1992

The formation and crystal structure of dihydronitidine and discussion of anticancer mechanism of nitidine cation.

The paper reports the formation and crystal structure of dihydronitidine, expounds the reasons and conditions of easily formed oxynitidine, and discusses anticancer mechanism of nitidine (cation). The crystallographic parameters of dihydronitidine are: space group P(2)1/n, a = 12.54(1), b = 9.148(5), c = 14.748(8) A, beta = 92.12(6)degrees, Z = 4. 4108 independent reflections were collected within the range of 3 degrees < or = 2 theta < or = 54 degrees, of which 2137 intensity data with I > or = 3 sigma (I) were used in the structural determination. The crystal structure has been refined by full matrix least-square method to a final R of 0.050.

Antineoplastic Agents, Phytogenic↗
PubMed2003

[Effect of inhibiting protein kinase C on calcium sensitivity of contractile apparatus of vascular smooth muscle during vasospasms of different origins].

The aim of the study was to investigate the role of protein kinase C (PKC) in changes in myofilament Ca(2+)-sensitivity of vascular smooth muscle cells (SMC) in rats at different vasospastic states: hypoxic pulmonary vasoconstriction, genetically determined hypertension, and hypertension resulted from ionizing radiation. All vasospastic states demonstrated rightward shifts in pCa-tension curves suggesting that myofilament Ca(2+)-sensitivity had increased. In chemically (beta-escin) skinned pulmonary artery, hypoxia-induced increase in myofilament Ca(2+)-sensitivity was completely abolished by PKC inhibitor chelerythrine. The similar results were demonstrated in skinned aorta SMC of spontaneously hypertensive rats where an increase in myofilament Ca(2+)-sensitivity was also abolished by PKC inhibitors chelerythrine and staurosporine. The chelerythrine partially inhibited myofilament Ca(2+)-sensitivity that had increased following gamma-radiation. The data suggest the key role of PKC activity in modulation of myofilament Ca(2+)-sensitivity in SMC. We conclude that PKC-mediated increase in myofilament Ca(2+)-sensitivity is one of the main mechanisms which contribute to the vasospasm of different genesis.

Actin Cytoskeleton↗
PubMed2004

CD3 receptor modulation in Jurkat leukemic cell line.

CD3 antigen is a crucial molecule in T cell signal transduction. Although its expression on cell surface is constitutive, dynamic regulation of TCR-CD3 level is probably the most important mechanism allowing T cells to calibrate their response to different levels of stimuli. In our study we examined the role of two main T cell signal transduction pathways in controlling the surface level of CD3 antigen, one based on protein kinase C activity and the other dependent on calcineurin. As an experimental model we used three clones derived from Jurkat cell line, expressing different levels of CD3 antigen surface expression: CD3(low) (217.6), CD3+(217.9) or CD3(low) (217.7). The cells were stimulated with PMA or ionomycin, acting directly on PKC and calcineurin, respectively. Prior to the stimulation cells were incubated with PKC inhibitor--chelerythrine or calcineurin blocker--cyclosporine A. Changes in CD3 surface expression were measured by flow cytometry. Only PMA and chelerythrine were able to change CD3 expression suggesting important involvement of PKC in the regulation of its expression. To confirm these findings, PKC activity was estimated in Jurkat clones. Our data demonstrated that Jurkat clones with different CD3 expression showed also different PKC activities, so we conclude that PKC-dependent pathway is the main way of controlling CD3 level on Jurkat clones.

Alkaloids↗
PubMed2004

Sanguinarine causes cell cycle blockade and apoptosis of human prostate carcinoma cells via modulation of cyclin kinase inhibitor-cyclin-cyclin-dependent kinase machinery.

Prostate cancer is the second leading cause of cancer-related deaths in males in the United States. This warrants the development of novel mechanism-based strategies for the prevention and/or treatment of prostate cancer. Several studies have shown that plant-derived alkaloids possess remarkable anticancer effects. Sanguinarine, an alkaloid derived from the bloodroot plant Sanguinaria canadensis, has been shown to possess antimicrobial, anti-inflammatory, and antioxidant properties. Previously, we have shown that sanguinarine possesses strong antiproliferative and proapoptotic properties against human epidermoid carcinoma A431 cells and immortalized human HaCaT keratinocytes. Here, employing androgen-responsive human prostate carcinoma LNCaP cells and androgen-unresponsive human prostate carcinoma DU145 cells, we studied the antiproliferative properties of sanguinarine against prostate cancer. Sanguinarine (0.1-2 micromol/L) treatment of LNCaP and DU145 cells for 24 hours resulted in dose-dependent (1) inhibition of cell growth [as evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay], (2) arrest of cells in G0-G1 phase of the cell cycle (as assessed by DNA cell cycle analysis), and (3) induction of apoptosis (as evaluated by DNA ladder formation and flow cytometry). To define the mechanism of antiproliferative effects of sanguinarine against prostate cancer, we studied the effect of sanguinarine on critical molecular events known to regulate the cell cycle and the apoptotic machinery. Immunoblot analysis showed that sanguinarine treatment of both LNCaP and DU145 cells resulted in significant (1) induction of cyclin kinase inhibitors p21/WAF1 and p27/KIP1; (2) down-regulation of cyclin E, D1, and D2; and (3) down-regulation of cyclin-dependent kinase 2, 4, and 6. A highlight of this study was the fact that sanguinarine induced growth inhibitory and antiproliferative effects in human prostate carcinoma cells irrespective of their androgen status. To our knowledge, this is the first study showing the involvement of cyclin kinase inhibitor-cyclin-cyclin-dependent kinase machinery during cell cycle arrest and apoptosis of prostate cancer cells by sanguinarine. These results suggest that sanguinarine may be developed as an agent for the management of prostate cancer.

Alkaloids↗
PubMed2004

IgA immune complex blunts the contraction of cultured mesangial cells through the inhibition of protein kinase C and intracellular calcium.

The effects of IgA immune complex (IgA-IC) on the contractile function of cultured mesangial cells were measured by the changes in planar surface area in response to treatment with agonists. Incubation of mesangial cells with IgA-IC for 24 hours significantly decreased the contractile responses to angiotensin II (10(-6) M) and phorbol 12-myristate 13-acetate (PMA, 10(-6) M). Pretreatment of mesangial cells with the protein kinase C (PKC) inhibitor, chelerythrine (10(-6) M), eliminated the difference in contractile responses to angiotensin II or PMA between the control and IgA-IC groups indicating IgA-IC may inhibit the activity of PKC. The contractile responses to ionomycin were not significantly different between IgA-IC treated and control mesangial cells, suggesting that the contractile machinery is not impaired by IgA-IC. Intracellular calcium, [Ca2+]i measured by changes in fura-2 level in response to ATP or bradykinin, was significantly inhibited in IgA-IC treated mesangial cells, compared to control cells. In contrast, treatment with thapsigargin did not result in significant differences in [Ca2+]i between IgA-IC and control mesangial cells, suggesting that a negligible role of endoplasmic reticulum in the effects of IgA-IC. Using PKC specific antibodies, IgA-IC significantly increased the particulate fraction of PKC-iota of mesangial cells to 141+/-13% of control, without significantly changing the protein content of PKC-alpha, -delta and -lambda in the cytosolic and particulate fractions. In summary, IgA-IC inhibits the contractile responses of cultured mesangial cells to agonists by inhibiting the activation of PKC and [Ca2+]i.

Alkaloids↗
PubMed2004

[Determination of protopine and isocorydine in root of Dactylicapnos scandens by HPLC].

OBJECTIVE: To establish a HPLC method for determination of protopine and isocorydine in root of Dactylicapnos scandens. METHOD: The separation was performed in a PHENOMENEX-C18 column with a mobile phase of methanol-0.2% phosphoric acid (adjusted to pH 7.0 with triethylamine)(50:50), The detection wavelength was at 254 nm and the flow rate was 0.8 mL x min(-1). RESULT: The average recovery of Protopine and Isocorydine was 97.9%, 98.6% respectively, and RSD 1.3%, 1.4%. CONCLUSION: This method is accurate, simple and reliable. It can be used for quality control of D. scandens.

Aporphines↗