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At least 19 recordsLinked to original sources
PubMed1987

Effects of continuous intravenous infusion of an ovine placental extract enriched in placental lactogen on plasma hormones, metabolites and metabolite biokinetics in non-pregnant sheep.

Continuous intravenous infusions of saline or of a placental extract containing ovine placental lactogen were given to three non-pregnant, non-lactating ewes over periods of 36 h, 1 week apart. During saline infusion no placental lactogen was detected in jugular vein plasma. but infusion of the placental extract raised the placental lactogen concentration from undetectable to 40-50 micrograms/l, similar to concentrations in ewes with one fetus on day 90 of pregnancy. By comparison with the saline control period, infusion of the placental extract consistently increased both plasma concentrations and irreversible loss of nonesterified fatty acids. Plasma concentrations of glucose and urea, but not irreversible loss of these metabolites, were consistently increased. Although the placental extract was not subjected to extensive purification, it was enriched in placental lactogen and contained no detectable contamination with insulin, prolactin or growth hormone. The results are suggestive of a role for placental lactogen in modifying metabolism and acting during pregnancy to provide nutrients for fetal metabolism.

Animals↗
PubMed1984

Modulation of mouse anti-SRBC antibody response by placental extracts.

Mouse placental extracts (PE) and corresponding Sephadex G-200 fractions were administered to isogeneic CBA mice along with an optimal immunizing dose of SRBC. Spleen cells were harvested 8 days later and transferred to CBA recipients, subsequently immunized with SRBC. The immunoregulatory activity of spleen cells from PE-treated donors was compared to cells from liver extract (LE)-treated controls or from mice immunized with SRBC only, using Cunningham's PFC direct and indirect tests. Within the dose range used, selective modulatory activities were obtained with cells from PE, but not from LE, treated mice, the latter being comparable to cell transfer effects from donors immunized with SRBC only. Spleen cells from animals injected with low doses of PE (0.25 to 4 mg per mouse) added to immunizing SRBC had a suppressive effect on the primary IgM response of recipients immunized against SRBC. In contrast, when SRBC were given to donor animals with higher doses of PE (8 to 13 mg), transferred spleen cells potentiated the IgM response of the recipients. These opposite suppressive and potentiating activities were found in distinct Sephadex G-200 fractions of 40 and 60 kDa, respectively. When the effect of PE treatment was tested within the same animal, the indirect secondary PFC response following a challenge with SRBC was significantly modified. We observed an overall suppression of the different isotypes after treatment with lower doses of PE or with its 40-kDa fraction. PE doses of 0.5 to 2 mg resulted in a stronger inhibition of IgM than IgG1 production. This phenomenon was also obtained with the 40 KDa fraction. IgG2 responses were significantly reduced by all doses of this fraction. In contrast, all doses of the 60-kDa fraction gave a strong stimulation of IgG2 and IgM responses and a constant suppression of the IgG1 response. This shows a clear dissociation between IgG1 and C'-fixing (IgM, IgG2) antibody classes as far as the influence of placental substances is concerned in their regulation. These data emphasize the relevance of isogeneic placental products as a useful physiological material capable of modulating xenogeneic immune responses (as well as allogeneic systems).

Animals↗
PubMed2002

Final report on the safety assessment of human placental protein, hydrolyzed human placental protein, human placental enzymes, human placental lipids, human umbilical extract, placental protein, hydrolyzed placental protein, placental enzymes, placental lipids, and umbilical extract.

Various proteins, lipids, or other extracts from human or other animal placentas are described as cosmetic ingredients. Human Placental Protein comprises protein derived from human placentas. Placental Protein is derived from animal placentas. Similarly, Human Placental Lipids and Placental Lipids are the lipid fractions from the same source materials. Hydrolyzed Human Placental Protein and Hydrolyzed Placental Protein are produced from the respective protein extracts by acid, enzyme, or other hydrolysis methods. Human Placental Enzymes and Placental Enzymes are enzymes obtained by aqueous extraction of human or other animal placental material. Human Umbilical Extract and Umbilical Extract are unspecified extracts of material from human or other animal umbilical cords. Different materials called Human Placental Extracts and Placental Extracts, assumed to contain estrogenic hormones or other biologically active substances, are not recognized as cosmetic ingredients, even though the use of these ingredients in cosmetics have been reported to the Food and Drug Administration (FDA). Human-derived ingredients are prohibited from use under the provisions of the European Union cosmetics directive based on concerns about transmission of human spongiform encephalopathies and viral diseases, for example, human immunodeficiency virus (HIV). Umbilical Extract has precedent for unrestricted use in Japan, except for certain products. Most of these ingredients are described as hair-conditioning agents and miscellaneous skin-conditioning agents, although the umbilical extracts function as biological additives in cosmetics. Of the human-derived ingredients, only Human Placental Protein is currently reported to be used. Animal-derived placental proteins, hydrolyzed proteins, lipids, and enzymes were all currently reported to be used. No current uses of the umbilical extracts were reported. Most of the available data relates to placental derivatives that appear to have estrogenic or other biological activity. The one clinical study that appears to utilize proteinaceous material only reported no irritant reaction. Clearly, the available data are insufficient to support safety of these ingredients in cosmetics. The additional data needed include (1) skin sensitization at concentration of use; (2) gross pathology and histopathology in skin and other major organ systems associated with repeated exposures, and dermal reproductive and developmental toxicity data; (3) photosensitization; (4) one genotoxicity assay in a mammalian system; if positive, then a 2-year dermal carcinogenicity study using National Toxicology Program (NTP) methods may be needed; (5) ocular toxicity, if available. Any studies should be done on all ingredients unless chemical analysis data show similarity among ingredients. Because there is confusion and concern about the use of substances with estrogenic or other biological activity in cosmetic formulations, it was concluded that none of these ingredients used in cosmetics should deliver any metabolic/endocrine activity. In addition, any current use of these ingredients should be free of detectable pathogenic viruses or infectious agents.

Animals↗
PubMed2003

Wound healing effects of porcine placental extracts on rats with thermal injury.

BACKGROUND: Placental extracts have been used as Chinese folk medicines to accelerate wound healing. However, the molecular mechanism of placental extracts on wound healing has not been identified. It is known that fibroblast growth factors (FGF) and transforming growth factors (TGF) are two key factors involved in wound healing. OBJECTIVES: To determine the molecular mechanism of placental extracts on wound healing. METHODS: The protein levels of both growth factors in rat skins with thermal injury were therefore studied to explore the molecular mechanism of placental extracts on wound healing. As cell proliferation is essential for wound healing, effects of placental extracts on fibroblast proliferation were also determined. RESULTS: As compared with the controls, the S phase of fibroblasts was significantly increased by 1.5-, 1.7- and 4.7-fold for 1, 10 and 30 mg mL(-1) of placental extracts, respectively. The increase of the S phase was not due to the minute amount of sex hormones in the placental extracts as the addition of equivalent amounts of hormones showed no increase of the S phase. In addition, a 2.5-fold increase of TGF-beta1 in wound skin biopsy was noticed with 30 mg mL(-1) of porcine placental extracts. The FGF levels in the wound skin receiving 30 mg mL(-1) of porcine placental extracts were also significantly increased compared with the controls. CONCLUSIONS: These ex vivo data support the observation that the application of 30 mg mL(-1) of placental extracts reduced the wound healing time by about 50%. To the best of our knowledge, this is the first report to explore the molecular mechanisms of porcine placental extracts on wound healing. These results may provide the insight into the potential use of porcine placental extracts as an alternative medicine for accelerating wound healing.

3T3 Cells↗
PubMed2004

Prostaglandins are responsible for the inhibition of breathing observed with a placental extract in fetal sheep.

We have previously observed that the infusion of a placental extract inhibits breathing movements in fetal sheep, suggesting that a placental factor may be responsible for the inhibition of fetal breathing. Our preliminary results suggested that a small peptide or a substance bound to a peptide was likely responsible for this inhibition. Since prostaglandins are found in high concentrations in the placenta, it is possible that they may be responsible for the inhibition of breathing observed with the placental extract. We hypothesized that if prostaglandins were the active factors in the placental extract, then inhibition of the production of placental prostaglandins should eliminate the activity of the extract. We infused untreated and indomethacin/ASA-treated placental extracts into the carotid artery of eight chronically instrumented fetal sheep continuously over 3 h. The concentration of all prostaglandins measured in the untreated placental extracts were significantly higher than in the indomethacin/ASA-treated extracts. Only the infusion of the untreated placental extract induced a significant decreased in the incidence of fetal breathing. Fetal plasma prostaglandins increased significantly only with the infusion of the untreated placental extracts. These findings suggest that the inhibition of breathing observed with the placental extract is likely related to prostaglandins.

Animals↗
PubMed1995

Effects of human placental extract on brain monoamines and monoamine oxidase activity in rats.

Human placental extract, an agent clinically used world-wide in a number of physiological anomalies, has been claimed to be effective in children of slow learners. Since the monoaminergic neurotransmitter systems in the brain play an important role in the processes of learning and memory, we examined the effects of human placental extract on the levels of norepinephrine, dopamine and serotonine in rat brain as an attempt to evaluate the possible underlying biochemical mechanism of action of the extract. We also determined the changes of brain monoamine oxidase (MAO) activity following placental extract treatment. The results showed that subchronic (5, 10, 15 or 20) administration of placental extract (2-4 ml/kg/day) had the effect of increasing all the monoamines and decreasing the MAO activity which could be the possible mode of action of the extract in slow learners.

Animals↗
PubMed2006

Effect of placental-extract gel and cream on non-healing wounds.

OBJECTIVE: To compare the effects of topical placental-extract gel and cream in the treatment of chronic non-healing wounds with regard to wound healing and discomfort during dressing change. METHODS: A sample of 120 patients attending the wound clinic at University Hospital, Varanasi, India, with wounds of more than six weeks' duration were enrolled into the study. They were alternately allocated to group A (topical application of placental-extract gel) or group B (placental-extract cream). Wound biopsy was performed, and swab culture and sensitivity were taken. Wound size was measured, and visual analogue scale (VAS) scores for pain and discomfort at dressing change were recorded at weekly follow-up in both groups. Biopsy was repeated after two weeks of treatment and sent for histopathological examination for assessment of angiogenesis in 25 cases from each group. RESULTS: One hundred patients completed the study. More than 50% wound healing was observed after eight weeks in 72% of group A patients and 74% of group B patients (p = 0.75). Microscopic angiogenesis grading system (MAGS) scores were similar in both groups (not statistically significant, p = 0.92). The VAS scores for pain and discomfort were lower in group B (statistically significant, p < 0.02). CONCLUSION: Placental-extract gel and cream are both effective topical agents for chronic non-healing wounds. However, there is less pain and discomfort during dressing change with the placental-extract cream, which we thus recommend for topical application in chronic non-healing wounds.

Administration, Cutaneous↗
PubMed2000

The effects of placental extracts from normotensive and preeclamptic women on vasoconstriction and oxidative metabolism.

OBJECTIVE: A circulating factor derived from the placenta has been implicated in the pathogenesis of preeclampsia. The aim of this study was to determine whether placental extracts from normotensive women and women with preeclampsia increase oxidative metabolism and histamine-induced vasoconstriction in porcine carotid artery. STUDY DESIGN: Placental extracts from normotensive women and women with preeclampsia were applied to porcine carotid artery, and oxidative metabolism was measured. Histamine-induced isometric force responses were also determined in the absence and presence of placental extracts. RESULTS: Application of placental extracts to porcine carotid artery caused a fall in oxygen tension, which reflects increased consumption. Extracts from placentas taken from women with preeclampsia caused a greater fall than those from normotensive women (0.117 +/- 0.026 vs 0.018 +/- 0.0024 micromol oxygen per milligram; P < or =.01). Histamine-induced contractions were potentiated by extracts from preeclampsia but not from those of women without hypertension. The maximal steady-state force values were 13,137 +/- 3647, 12,921 +/- 3684, and 21,673 +/- 7189 N/m(-2) for control, normotensive, and preeclamptic samples at 10-micromol/L histamine (P < or =.05, compared with control placental extracts). CONCLUSIONS: Placental extracts from women with preeclampsia cause a greater stimulation of porcine artery oxygen consumption and exacerbation of histamine-induced vasoconstriction than extracts from normotensive women.

Animals↗
PubMed1983

The ability of placental extracts to modulate a direct PFC response to SRBCs in mice.

Placental extracts were injected in conjunction with sheep or pigeon RBC to CBA female mice. Spleen cells from these animals were then transferred to isogeneic recipients. The immune response of these recipients, actively immunized towards the immunogen used for priming of cell donors, was studied. (1) It was shown that placental extracts were most efficient in inducing suppressor cell activity in a direct (IgM) plaque-forming assay when injected simultaneously with the immunogen used for cell donor priming. (2) Suppressor cells were generated both in anti-SRBC and anti-PRBC reactions and suppressed the corresponding IgM response after transfer to isogeneic recipients. (3) Combined experiments consisting of the transfer of cells, primed by either SRBC or PRBC, into recipients immunized with a mixture of both immunogens, resulted in a selective suppression of the response directed against the type of RBCs used for the induction of suppressor cells. Results are discussed in the light of previous experiments from this and other laboratories, which showed suppressor effects of placental extracts operating in transplantation systems.

Animals↗
PubMedDate not supplied

Evidence of endothelial cytotoxic compounds in placental extracts from preeclamptic women.

OBJECTIVE: To determine whether placenta and plasma of preeclamptic women contain factors that cause endothelial cell damage. METHODS: Placental extracts and plasma from preeclamptic and normotensive women were added to cultures of normal human umbilical vein endothelial cells and their effect on their viability, was determined by MTT reduction and 51chromium release. RESULTS: Placental extracts from normotensive and preeclamptic women were cytotoxic to endothelial cells, but not the plasma from both groups. Mean +/- standard deviation values of cytotoxicity index in preeclamptic and normotensive placental extracts using the MTT reduction were 70.3 +/- 6.76% and 51.4 +/- 8.81%, respectively, showing a significant difference (P < .0001). Using the 51chromium-release assay, preeclamptic placental extracts showed cytotoxic effects of 87.6 +/- 13.47% compared with 17 +/- 20.60% in control patients. The cytotoxic activity decreased after trypsin digestion and heat treatment in both groups. CONCLUSIONS: A cytotoxic factor to endothelial cells in placental extracts of preeclamptic women was identified. This compound is thermolabile and sensitive to trypsin digestion.

Cells, Cultured↗
PubMed1988

Stimulation of thymidine incorporation in keratinocytes by insulin, epidermal growth factor, and placental extract: comparison with cell number to assess growth.

The results of a thymidine incorporation assay were compared with direct measurement of cell number in assessment of proliferative growth of human keratinocytes in monolayer culture. Keratinocytes were cultured in supplemented MCDB 153 medium in 0.1 mM Ca2+, and plated in 24-well trays. The ability of insulin, placental extract, and epidermal growth factor to enhance growth and thymidine incorporation were compared. Autoradiography was performed to determine the percentage of cells with labeled nuclei. Epidermal growth factor increased thymidine incorporation under the conditions of the assay, and placental extract increased incorporation by up to 50-fold, since the control cells plated in the absence of epidermal growth factor and other growth factors survived but proliferated minimally. Both cell number and thymidine incorporation showed similar concentration dependence upon insulin and placental extract. If placental extract was added to cells plated 28 h earlier, incorporation was maximal after 17 h in the presence of the extract. If cells were plated in the presence of the extract, 85% of nuclei were shown by autoradiography to be labeled after 23 h, but only 24% of nuclei were labeled in the absence of the extract. A plating density of 10(4) cells/2-cm2 well was optimal. The assay permits rapid identification of growth-promoting fractions without prolonged growth periods, and is a valid indicator of these agents in keratinocyte cultures.

Autoradiography↗
PubMed2004

A trial to determine the role of placental extract in the treatment of chronic non-healing wounds.

OBJECTIVE: To investigate the effect of topical placental extract in the treatment of non-healing wounds. METHOD: One hundred patients attending the wound clinic at University Hospital, Varanasi, India, with wounds of more than six weeks' duration were recruited. Fifty patients were treated with placental extract, and 50 were controls. Wound biopsy and swab culture and sensitivity were performed and the area surrounding the wound was X-rayed. Wound size was measured and the rate of epithelialisation assessed at weekly follow-ups. In nine cases biopsies were repeated after two weeks of treatment and sent for histopathological examination, including angiogenesis. RESULTS: Thirty patients dropped out, leaving 40 cases in the treatment group and 30 in the control group. Over an eight-week period, 27 patients (67.5%) in the treatment group showed more than 50% epithelialisation, compared with only seven patients (23.3%) in the control group. CONCLUSION: Placental extract has a beneficial role to play as a topical agent in the management of chronic non-healing wounds.

Adult↗
PubMed2000

Effects of human placental extract on chemical and thermal nociception in mice.

Several reports indicate that pregnancy and parturition are associated with elevated maternal pain thresholds to noxious stimuli. The objective of this study was to examine whether the human placental extract, a clinically used preparation, can inhibit experimental nociception. Nociception was assessed in mice using acetic acid-induced writhing and hot-plate tests. The human placental extract (200 and 400 mg/kg, i.p.) elicited dose-related antinociception in the acetic acid-induced writhing test. Furthermore, it (200 mg/kg, i.p.) potentiated the morphine-induced antinociception (1.25 mg/kg, s.c.). In the hot-plate test, the human placental extract (100, 200 and 400 mg/kg, i.p.) per se, displayed no significant antinociception but potentiated the duration of morphine (10 mg/kg, s.c.) analgesia. The potentiation by the extract of the morphine-induced antinociception in both acetic acid and hot-plate tests was, however, found to be naloxone sensitive. Mice treated with the extract (400 mg/kg, i.p.) neither manifested any overt behavioural change in the open-field test nor demonstrated significant influence on pentobarbital sleeping time, suggesting that it has no central depressant or sedative activity. The data provide evidence to show that the human placental extract has a peripheral analgesic property possibly mediated by an opioid mechanism.

Animals↗