The complement system as well as the coagulation system has fundamental clinical implications in the context of life-threatening tissue injury and inflammation. Associations between both cascades have been proposed, but the precise molecular mechanisms remain unknown. The current study reports multiple links for various factors of the coagulation and fibrinolysis cascades with the central complement components C3 and C5 in vitro and ex vivo. Thrombin, human coagulation factors (F) XIa, Xa, and IXa, and plasmin were all found to effectively cleave C3 and C5. Mass spectrometric analyses identified the cleavage products as C3a and C5a, displaying identical molecular weights as the native anaphylatoxins C3a and C5a. Cleavage products also exhibited robust chemoattraction of human mast cells and neutrophils, respectively. Enzymatic activity for C3 cleavage by the investigated clotting and fibrinolysis factors is defined in the following order: FXa > plasmin > thrombin > FIXa > FXIa > control. Furthermore, FXa-induced cleavage of C3 was significantly suppressed in the presence of the selective FXa inhibitors fondaparinux and enoxaparin in a concentration-dependent manner. Addition of FXa to human serum or plasma activated complement ex vivo, represented by the generation of C3a, C5a, and the terminal complement complex, and decreased complement hemolytic serum activity that defines exact serum concentration that results in complement-mediated lysis of 50% of sensitized sheep erythrocytes. Furthermore, in plasma from patients with multiple injuries (n = 12), a very early appearance and correlation of coagulation (thrombin–antithrombin complexes) and the complement activation product C5a was found. The present data suggest that coagulation/fibrinolysis proteases may act as natural C3 and C5 convertases, generating biologically active anaphylatoxins, linking both cascades via multiple direct interactions in terms of a complex serine protease system.

The complement system as a main column of innate immunity and the coagulation system as a main column in hemostasis undergo massive activation early after injury. Interactions between the two cascades have often been proposed but the precise molecular pathways of this interplay are still in the dark. To elucidate the mechanisms involved, the effects of various coagulation factors on complement activation and generation of anaphylatoxins were investigated and summarized in the light of the latest literature. Own in vitro findings suggest, that the coagulation factors FXa, FXIa and plasmin may cleave both C5 and C3, and robustly generate C5a and C3a (as detected by immunoblotting and ELISA). The produced anaphylatoxins were found to be biologically active as shown by a dose-dependent chemotactic response of neutrophils and HMC-1 cells, respectively. Thrombin did not only cleave C5 (Huber-Lang et al. 2006) but also in vitro-generated C3a when incubated with native C3. The plasmin-induced cleavage activity could be dose-dependently blocked by the serine protease inhibitor aprotinin and leupeptine. These findings suggest that various serine proteases belonging to the coagulation system are able to activate the complement cascade independently of the established pathways. Moreover, functional C5a and C3a are generated, both of which are known to be crucially involved in the inflammatory response.

As a crucial element of innate immunity, the complement cascade becomes activated after severe trauma. Regulation of the complement cascade and protection against complement-mediated tissue destruction is provided by a selection of soluble and membrane-bound complement regulatory proteins (CRegs). To date, the leukocyte expression profile of CRegs in multiple injured patients is unknown. In the present study, expression of CRegs and the C5a receptor (CD88) was analyzed on neutrophils, monocytes, and lymphocytes by flow cytometry. Whole blood samples were obtained from healthy volunteers (n = 16) or multiple injured patients (n = 12) on admission in the emergency department and 4, 12, 24, 120, and 240 h after trauma. The content of CRegs and CD88 on leukocytes was significantly altered posttrauma: CD55 (decay accelerating factor) displayed a time-dependent, elevated expression pattern on neutrophils and monocytes, but not on lymphocytes. CD59 (membrane attack complex inhibitor) expression was significantly increased on neutrophils and monocytes at the time of admission and after 5 to 10 days in lymphocytes. CD46 (membrane cofactor protein) was significantly down-regulated in all three cell types posttrauma. CD35 (complement receptor 1) expression on neutrophils was initially decreased, whereas monocytes presented a significant increase in CD35 expression. CD35 on lymphocyte remained unchanged throughout the observation period. CD88 expression was considerably reduced on leukocytes between 0 and 240 h after injury. CD59, CD46, and CD88 expression values on neutrophils reversely correlated with severity of injury. In summary, expression profiles of CRegs and CD88 on leukocytes are specifically altered after polytrauma in humans, indicating a trauma-induced "complementopathy."

Plants from the start are being used for the welfare of human and animals. About 25,000 biological active compounds are reported by different scientists. Plants itself are a complete treatment bioagent. People are still using plants and their decoction for different diseases. Saussurea lappa Clarke is the member of family Compositae. This plant is famous due to its high medical importance. The plant is commonly named as Kuth root or costus and has wide use for anticancer, antiulcer, hepatoprotective, anti-viral, anticonvulsant, antiarthritic, activities. Biologically active substance of in this plant is lactone cynaropicrin, dehydrocostus, germacrene, lappadilactone. This plant can be used to extract such bioactive compounds which can help the scientist to discover new and potential drugs. Due to such chemical composition and medicinal importance this review has been prepared for the awareness of the people to conserve their medicinal plants which can be used for potential drug discovery.

With the progression of nanotechnology, the use of nanoparticles (NPs) in consumer products has increased dramatically and green synthesis is one of the cheapest and eco-friendly methods to obtain non-hazardous NPs. In the current research zinc (Zn) NPs synthesis was carried out by using the fresh and healthy leaves of Mentha arvensis L. followed by characterisation through ultraviolet (UV)-visible spectroscopy, X-ray diffraction (XRD) and scanning electron microscopy (SEM). UV-visible spectroscopy confirmed the green synthesis of ZnNPs, while XRD confirmed the size of NPs, which was 30-70 nm. SEM shows that the shape of ZnNPs was irregular. The effects of green synthesised NPs on two different varieties of Brassica napus were evaluated. Exposure to ZnNPs (5, 15, and 25 mg/l −1) caused a significant increase in root and shoot length of B. napus. The application of NPs significantly improved plant germination and triggered the production of secondary metabolite and antioxidant enzymes. ZnNPs showed a significant increase in chlorophyll, superoxide dismutase, total flavonoid content (TFC) and antioxidant enzymes while total phenolic content was decreased when TFC increased. Thus, it has been concluded from the current study that ZnNPs may possibly trigger the production of antioxidant enzymes and various biochemical compounds.