Studi ini bertujuan untuk membuat ekstrak air daun selasih untuk penyembuhan flu dan demam. Metode yang digunakan adalah eksperimen dan uji aktivitas katalik secara langsung. Tahapan pertama yang di lakukan adalah pembuatan ekstrak dari daun selasih. Uji aktivitas langsung dilakukan dengan variasi pemakaian setiap 15 menit sehari. Hasil eksperimen membuktikan bahwa remasan daun selasih dapat menyembuhkan flu dan hidung tersumbat. Kondisi optimum terhadap ekstrak daun selasih dapat dilihat 1 hari dengan berkali-berkali pemakaian. Penyembuhan ini di duga karena aktivitas/zat aktif yaitu asam fenolat yang memiliki aktivitas anti bakteri , anti inflamasi, anti kanker, dan anti virus.
Background Postoperative pain management is a critical aspect of patient care. The inflammatory state of the post-sternotomy surgical wound sensitizes nerve endings, causing pain. Unrelieved or improperly managed pain compromises wound healing. Peripheral opioid receptors play a major role in analgesia, particularly under inflammatory conditions where both opioid receptor expression and efficacy are increased. Leukocytic opioid peptides include β-endorphin (END), met-enkephalin (ENK), and dynorphin-A (DYN), with END and ENK being predominant. Methodology/Principal Findings This work represents the first study of inflammatory cells collected from post-sternotomy wounds of patients undergoing cardiac surgery including coronary artery bypass grafting (CABG). Wound fluid (WF) and cells were collected from sternal wounds using a JP Blake drain at 24, 48, and 72 hours post sternum closure. Anti-CD15 staining and flow cytometry revealed that polymorphonuclear neutrophils (PMN) are the predominant cells present in wound fluid collected post-surgery. Compared to peripheral blood (PB) derived PMN, significant increases in CD177+/CD66b+ PMN were observed suggesting activation of wound-site PMN. Such activation was associated with higher levels of opioid peptide expression in PMN derived from WF. Indeed, increased level of opioid peptides in sternal wound environment was noted 72 h post-surgery. We demonstrate that WF contains factors that can significantly induce POMC transcription in human PMNs. IL-10 and IL-4 were abundant in WF and both cytokines significantly induced POMC gene expression suggesting that WF factors such as IL-10 and IL-4 contribute towards increased opioid peptide expression in wound-site PMN. Conclusions/Significance This approach provided a unique opportunity to study the cross-talk between inflammation and opioid peptides in PMN at a sternotomy wound-site. Wound-site PMN exhibited induction of END and ENK. In addition, sternal wound fluid significantly induced END expression in PMN. Taken together, these data constitute first clinical evidence that human wound-site PMNs are direct contributors of opioids at the sternal wound-site.
The insulin granule integral membrane protein marker phogrin-green fluorescent protein was co-localized with insulin in Min6B1 β-cell secretory granules but did not undergo plasma membrane translocation following glucose stimulation. Surprisingly, although expression of a dominant-interfering dynamin mutant (Dyn/K44A) inhibited transferrin receptor endocytosis, it had no effect on phogringreen fluorescent protein localization in the basal or secretagogue-stimulated state. By contrast, co-expression of Dyn/K44A with human growth hormone as an insulin secretory marker resulted in a marked inhibition of human growth hormone release by glucose, KCl, and a combination of multiple secretagogues. Moreover, serial pulse depolarization stimulated an increase in cell surface capacitance that was also blocked in cells expressing Dyn/K44A. Similarly, small interference RNA-mediated knockdown of dynamin resulted in marked inhibition of glucose-stimulated insulin secretion. Together, these data suggest the presence of a selective kiss and run mechanism of insulin release. Moreover, these data indicate a coupling between endocytosis and exocytosis in the regulation of β-cell insulin secretion.
Richard J. Hendrickson, Charles R. Cappadona, E. Yankah
et al.
This study addresses the effect of sustained increased pulsatile flow on nitric oxide synthase (NOS) and cyclooxygenase (Cox) expression and activity in co-cultured endothelial cells (EC) and vascular smooth muscle cells (SMC). Using a perfused transcapillary co-culture system which permits the chronic exposure of cultured EC and SMC to physiological shear stresses, co-cultures were exposed to step-wise increases in flow up to: (i) 2 ml/min (low flow: 0.5 dyn/cm2): or (ii) 44 ml/min (high flow: 15 dyn/cm2) and maintained for 72 h before SMC and EC were harvested separately. There was no NOS activity or protein expression in co-cultured SMC under flow conditions. There was a significant increase in eNOS activity in co-cultured EC under high flow conditions, compared to low flow, which correlated with an increase in eNOS expression and mRNA levels. The flow-induced increase in eNOS activity was potentiated by indomethacin treatment, suggesting a modulatory role for a cyclooxygenase product. Prostacyclin levels in co-culture perfusate were significantly elevated under high flow conditions. While both co-cultured EC and SMC expressed cyclooxygenase (Cox-I and Cox-II), they were differentially regulated by pulsatile flow, EC Cox-I and Cox-II protein expression were both decreased. Indomethacin treatment increased the expression of both Cox-I and Cox-II in co-cultured SMC under high flow conditions. We conclude that sustained increases in pulsatile flow maintain elevated eNOS and Cox protein expression and activity in EC while decreasing Cox expression in co-cultured SMC. These data suggest that regulation of these pathways may contribute to flow-induced vascular remodeling in vivo.