Evaluation of anti-inflammatory, immunomodulatory, chemopreventive and wound healing potentials from Schinus terebinthifolius methanolic extract

Inflammatory and genetic alterations are related to the development of chronic diseases such as cancer. Schinus terebinthifolius Raddi, Anacardiaceae, is used in folk medicine to treat inflammation, wounds and tumors. This study evaluated the anti-inflammatory, immunomodulatory, chemopreventive, and wound healing potentials of the methanolic extract from the leaves of Schinus terebinthifolius. The chemical composition of the extract was characterized using preliminary analytical LC methods. The results showed that the anti-inflammatory activity of the methanolic extract was similar to that of dexamethasone for edema reduction. Also, it inhibited the leukocyte migration into the air pouch and decreased plasma extravasation. In addition, the methanolic extract showed a healing action similar to that observed with collagenase. The methanolic extract is not genotoxic nor mutagenic, and in contrast it has chemopreventive activity, which elicits a high percentage of damage reduction by comet and micronucleus assay, preferably by bioantimutagenic action. The methanolic extract induced apoptosis and enhanced splenic phagocytosis in animals treated with cyclophosphamide. The methanolic extract contents, resolved by LC, include phenolic acid and flavonoids. Our results suggest a therapeutic potential for the methanolic extract.

Testis morphometry and kinetics of spermatogenesis in the feral pig (Sus scrofa).

The feral pig (Sus scrofa sp) also known as Monteiro pig, originated from a domestic pig breed that was introduced into Pantanal region in Brazil in the eighteenth century. Although the feral pig has commercial potential, there are few reports in the literature concerning the reproductive biology of this species. Therefore, the aim of this study was to further describe the feral pig testis parenchyma as well as characterize the stages of the seminiferous epithelium cycle by tubular morphology method, and to evaluate the number of differentiated spermatogonia generations in this species. Eight sexually mature feral pigs were analyzed. Fragments of testes were embedded in plastic resin and used to prepare slides for morphometrical studies. It was concluded that the feral pig has six generations of differentiated spermatogonials (A1, A2, A3, A4, In, B) and that the cellular composition in the eight stages of the seminiferous epithelium cycle of these animals were very similar to those reported in species of suidae and tayssuidae already studied.

Blood-tissue barriers: morphofunctional and immunological aspects of the blood-testis and blood-epididymal barriers.

The blood-testis barrier (BTB) is known for its ability to create an immune privilege site in the seminiferous epithelium, but less is known of the blood-epididymal barrier (BEB). It is already established that the fully functional BTB and BEB are much more complex and consist of anatomical/physical (tight junctions, basolateral and apical membranes), physiological and immunological components, which are all necessary to make a functioning barrier in the testis and epididymis. However, comparative data for metazoans suggest that an effective Sertoli cell barrier is not entirely necessary for the development of germ cells during spermatogenesis or that our knowledge about the barrier structure/function in metazoans is still immature. This chapter compares the unique barrier formed by the Sertoli cells of the testis to that formed by the apical junctional complexes of the epididymal epithelium.

Prenatal plus postnatal exposure to Di(n-Butyl) phthalate and/or flutamide markedly reduces final sertoli cell number in the rat.

Androgens may be important regulators of Sertoli cell (SC) proliferation perinatally, with implications for the testicular dysgenesis syndrome (TDS) hypothesis. Fetal exposure of rats to 500 mg/kg . d di(n-butyl) phthalate (DBP) reduces fetal testosterone production and SC number at birth, but SC number recovers to normal by postnatal d (Pnd)25. It is unclear when and how SC proliferation is affected prenatally by DBP exposure or when and how postnatal compensation occurs. This study addressed these questions and investigated whether continued maternal exposure to DBP or to flutamide from Pnd1-Pnd15 could prevent SC number compensation, because this would have implications for how sperm counts might be lowered in TDS. DBP exposure attenuated SC proliferation by 7-18% throughout embryonic d (e)15.5-e21.5 (P < 0.05 at e21.5). After birth, SC proliferation increased significantly (>1.5-fold) between Pnd6 and Pnd10 in prenatally DBP-exposed animals, explaining the compensation. Continued maternal administration of DBP after birth attenuated (19% reduction) SC number compensation at Pnd25 and maternal administration of flutamide (100 mg/kg . d) to prenatally DBP-exposed animals was even more effective (42% reduction), suggesting the postnatal compensatory increase in SC proliferation after prenatal DBP exposure is androgen dependent. SC maturation (Pnd25) was unaffected, based on analysis of expression of key proteins, but lumen formation/expansion was attenuated in parallel with treatment-induced reduction in SC number. Our results provide further evidence that perinatal SC proliferation is androgen dependent and, importantly, show that similar exposure of mothers to antiandrogenic chemicals before birth and during lactation reduces final SC number, with implications for the origin of low sperm counts in TDS.