Cinnamoyl, p-coumaroyl, feruloyl, caffeoyl
aloesin, and related compounds were isolated from Aloe species. The antiinflammatory and antioxidative activities of these compounds were examined based on the structure-activity relationship. It was suggested that the bioactivities may link to acyl
ester groups in
aloesin, together with those of
aloesin-related compounds. However, investigations using the
contact hypersensitivity response indicated a preventive effect of
aloesin on the UV-B-induced immune suppression. Furthermore,
aloesin inhibited
tyrosine hydroxylase and
dihydroxyphenylalanine (
DOPA) oxidase activities of
tyrosinase from normal human melanocyte cell lysates. These results show that
aloesin prevents not only UV-B-induced immune suppression, but also could be a positive pigment-altering agent for cosmetic application. In preclinical study, aloe extract was investigated using phagocytosis and
nitroblue tetrazolium chloride (NBT) reduction in adult
bronchial asthma, and high molecular-weight materials, such as
polysaccharide and
glycoprotein fractions, were identified as active ingredients. The neutral
polysaccharides,
aloemannan and
acemannan showed antitumor, antiinflammatory and immunosuppressive activities, and
glycoprotein fractions with bradykinindegrading and cell proliferation-stimulating activities were identified from the nondialysate fraction of the gel part of Aloe species. Verectin fractionated from
Aloe vera gel was examined biochemically and immunochemically, and verectin antibody was used in the appraisal of commercial
Aloe vera gel products. It was reported that
aloesin stimulates the proliferation of cultured human
hepatoma SK-Hep 1 cells. Thus
aloesin, related compounds, and high molecular-weight materials, such as
aloemannan and verectin, may act in concert to exert therapeutic properties for
wounds,
burns and
inflammation. The biodisposition of fluoresceinylisothiocyanate (
FITC)--labeled
aloemannan (
FITC-AM) with the homogenate from some organs in mice was demonstrated, and
FITC-AM was metabolized to a smaller molecule (MW 3000) by the large intestinal microflora in feces. The modified aloe
polysaccharide (MW: 80000) with
cellulase under restricted conditions, immunologically stimulated the recovery of UV-B-induced tissue in jury. Thus the modified
polysaccharides of
aloemannan, together with
acemannan (MW: about 600000), are expected to participate in
biological activity following
oral administration. The effects of
tanshinone VI, a
diterpenoid isolated from Salvia miltiorrhiza, on the heart are reviewed. First, the effects on the posthypoxic recovery of contractile function of perfused rat hearts were examined.
Hypoxia/reoxygenation induced a release of
purine nucleosides and bases (
ATP metabolites) and resulted in little recovery of contractile force of reoxygenated hearts. Pretreatment of the perfused heart with 42 nM
tanshinone VI under hypoxic conditions attenuated the release of
ATP metabolites during
hypoxia/reoxygenation. Treatment with
tanshinone VI enhanced the posthypoxic recovery of myocardial contractility. These results show that
tanshinone VI may protect the heart against
hypoxia/reoxygenation injury and improve the posthypoxic cardiac function. Second, the effects of
tanshinone VI on in vitro myocardial remodeling were examined. Cardiomyocytes and cardiac fibroblasts were isolated from neonatal rat hearts, and simultaneously prepared
insulin-like growth factor-1 (IGF-1) induced the
hypertrophy of cardiomyocytes.
IGF-1 increased the
collagen synthesis of cardiac fibroblasts, that is, in vitro
fibrosis. The
hypertrophy of cardiomyocytes was attenuated in the presence of
tanshinone VI in the culture medium. The
fibrosis of cardiac fibroblasts was decreased by treatment with
tanshinone VI. When
tanshinone VI was added to cardiac fibroblast-
conditioned medium, the medium-mediated
hypertrophy of cardiomyocytes was also attenuated. These results show that
tanshinone VI may attenuate in vitro cardiac remodeling. The series of studies has shown that
tanshinone VI protects the myocardium against
hypoxia/reoxygenation injury and attenuates progression of in vitro myocardial remodeling, suggesting that
tanshinone VI is a possible agent for the treatment of
cardiac disease with contractile failure.