OBJECTIVETo investigate the effects of Aloe vera extract (AV) on mitochondria in rat pheochromocytoma (PC12) cells and rat brain and to study the mechanism of its neuroprotection.

METHODAfter treatment, the morphology of PC12 cells was observed under microscope, the activity of mitochondria in PC12 cells was measured by MTT method, and the mitochondrial membrane potential (MMP) in PC12 cells was detected by JC-1 method. The mitochondrial function in rat brain was detected by resazurin method. The production of malondialdehyd (MDA) in rat brain mitochondria was tested by thiobarbaturic acid (TBA) assay.

RESULTAV could improve mitochondrial damage induced by azide sodium (NaN3) in PC12 cells. The viability of PC12 cells treated with NaN364 mmol x L(-1) for 4 h decreased by 47.8%, and AV at 1 and 10 mg x L(-1) could respectively increase the viability of NaN3-treated cells by 16.7% (P < 0.05) and 22.3% (P < 0.01). MMP in PC12 cells in AV 1 and 10 mg x L(-1) group was significantly higher than that of NaN3-treated group (P < 0.05). AV also protected the structure and function of mitochondria in rat brain. AV at 10 mg x L(-1) had protective effect on mitochondria function impair induced by NaN3 (P < 0.01). AV 1 and 10 mg x L(-1) markedly inhibited the lipid peroxidation of brain mitochondria induced by Fe2+ -cysteine (P < 0.05, P < 0.01).

CONCLUSIONAV has protective effects on mitochondria of neuronal cells and rat brain.

Aloe ; chemistry ; Animals ; Brain ; drug effects ; metabolism ; Lipid Peroxidation ; drug effects ; Male ; Malondialdehyde ; metabolism ; Mitochondria ; drug effects ; metabolism ; Neurons ; drug effects ; metabolism ; PC12 Cells ; Plant Extracts ; pharmacology ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Sodium Azide ; pharmacology

AIMTo seek for new components as BACE inhibitors from Aloe arborescens.

METHODSThe chemical constituents were isolated by chromatographic methods and their structures were elucidated on the basis of spectral analysis.

RESULTSEight compounds were isolated and their structures identified as 6'-O-isobutyryl aloenin A (1), aloenin A (2), aloe-emodin (3), (E)-2-acetonyl-8-(2'-O-feruloxyl)-beta-D-glucopyranosyl-7-methoxy-5-methyl-chromone (4), 7-O-methylaloeresin A (5), babarloin A (6), elgonica-dimer A (7), and elgonica-dimer B (8), separately.

CONCLUSIONCompound 1 is a new compound, and compound 4 was isolated from A. arborescens for the first time. Pharmacological tests indicated that 2, 4, 5 and 6 have moderate inhibitory active on BACE.

Aloe ; chemistry ; Amyloid Precursor Protein Secretases ; antagonists & inhibitors ; metabolism ; Anthraquinones ; chemistry ; isolation & purification ; pharmacology ; Aspartic Acid Endopeptidases ; antagonists & inhibitors ; metabolism ; Chromones ; chemistry ; isolation & purification ; pharmacology ; Enzyme Inhibitors ; chemistry ; isolation & purification ; pharmacology ; Glucosides ; chemistry ; isolation & purification ; pharmacology ; Humans ; Molecular Conformation ; Molecular Structure ; Plant Components, Aerial ; chemistry ; Plant Extracts ; chemistry ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Pyrones ; chemistry ; isolation & purification ; pharmacology

Aloe is one of the leading products used in phytomedicine. Several cases of aloe-induced toxic hepatitis have been reported in recent years. However, its toxicology has not yet been systematically described in the literature. A 21-year-old female patient was admitted to our hospital with acute hepatitis after taking an aloe vera preparation for four weeks. Her history, clinical manifestation, laboratory findings, and histological findings all led to the diagnosis of aloe vera-induced toxic hepatitis. We report herein on a case of acute toxic hepatitis induced by aloe vera.
Adult ; Aged ; Alanine Transaminase/blood ; Alkaline Phosphatase/blood ; Aloe/*chemistry/metabolism ; Drug-Induced Liver Injury/*diagnosis/etiology/pathology ; Female ; Humans ; Liver/pathology ; Male ; Middle Aged ; Plant Extracts/*adverse effects/*chemistry ; Splenomegaly/diagnosis ; Tomography, X-Ray Computed ; Young Adult

OBJECTIVETo investigate the effect of aloe polysaccharides pretreatment on the cerebral inflammatory response and lipid peroxidation in severe hemorrhagic shock rats first entering high altitude.

METHODSForty healthy male SD rats weighing 250-300 g were randomly divided into 5 groups (n = 8 each): sham group, shock group, AP group was further divided into 3 subgroups (AP1 0.75 mg/kg; AP2 1.50 mg/kg; AP3 3.00 mg/kg). The different doses AP were given iv respectively at 30 min before hemorrhagic shock. The mean blood pressure (MAP) was maintained at (35 ± 5) mmHg (1 mmHg = 0.133 kPa) for 60 minutes. The animals were killed at 2 hours after resuscitation. Blood samples were obtained from femoral artery for detecting tumor necrosis factor α (TNF-α), IL-6 and IL-10 concentrations; the frontal and parietal lobes brain and the hippocampus were separated from brain tissues on the ice for detecting superoxide dismutase (SOD) activity and myeloperoxidase (MPO) activity, malondialdehyde (MDA) concentration, brain Wet-dry weight ratio (W/D).

RESULTSCompared with sham group, hemorrhagic shock significantly increased serum TNF-α ((76 ± 11) ng/L), IL-6 ((1303 ± 141) ng/L) and IL-10 concentrations ((95 ± 14) ng/L), MPO activity ((20.72 ± 2.28)×10(-2) U/g) and MDA concentration ((80 ± 13) nmol/mgprot) in the brain tissue and brain W/D (6.21 ± 0.18) (t = 6.928 - 14.565, P < 0.05), while SOD activity ((56 ± 11) U/mgprot) decreased significantly (t = -5.374, P < 0.05). There were no significant difference between shock and AP1 groups. AP2 group significantly inhibited hemorrhagic shock-induced increase serum TNF-α ((54 ± 12) ng/L), IL-6 ((846 ± 78) ng/L) and IL-10 concentrations ((66 ± 11) ng/L), MPO activity ((13.13 ± 1.23)×10(-2) U/g) and MDA concentration ((56 ± 9) nmol/mgprot) in the brain tissue and brain W/D (5.71 ± 0.18) (t = -6.905 - -3.357, P < 0.05), while SOD activity ((86 ± 12) U/mgprot) increased significantly compared to shock group (t = 4.240, P < 0.05). There were no significant difference between AP2 and AP3 groups.

CONCLUSIONAP pretreatment can attenuate the cerebral ischemia and reperfusion injury in severe traumatic-hemorrhagic rats first entering high altitude through inhibiting systemic inflammatory response and leukocyte aggregation and lipid peroxidation in the brain.

Aloe ; chemistry ; Altitude ; Animals ; Brain ; metabolism ; pathology ; Brain Ischemia ; drug therapy ; prevention & control ; Disease Models, Animal ; Interleukin-10 ; blood ; Interleukin-6 ; blood ; Lipid Peroxidation ; Male ; Malondialdehyde ; metabolism ; Polysaccharides ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; drug therapy ; prevention & control ; Shock, Hemorrhagic ; metabolism ; pathology ; Superoxide Dismutase ; metabolism ; Tumor Necrosis Factor-alpha ; blood