2. Apoptosis Cytoskeleton Cell Cycle/DNA Damage Membrane Transporter/Ion Channel Neuronal Signaling
  3. Apoptosis MDM-2/p53 PAK Calcium Channel
  4. Sennoside

Sennoside is an orally active apoptosis inducer and stimulant laxative, found in Senna (Cassia angustifolia). Sennoside induces overexpression of wild-type p53 and p21/WAF as part of pathways mediating colonic epithelial cell apoptosis. Sennoside stimulates colonic peristalsis, reverses net water, sodium, chloride absorption to secretion and enhances potassium and calcium secretion. Sennoside increases paracellular permeability to small molecules, accelerates colon transit and softens fecal pellets. Sennoside can be used for the research of constipation, melanosis coli, and colorectal cancer.

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Sennoside

Sennoside Chemical Structure

CAS No. : 517-43-1

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Sennoside Related Antibodies

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Description

Sennoside is an orally active apoptosis inducer and stimulant laxative, found in Senna (Cassia angustifolia). Sennoside induces overexpression of wild-type p53 and p21/WAF as part of pathways mediating colonic epithelial cell apoptosis. Sennoside stimulates colonic peristalsis, reverses net water, sodium, chloride absorption to secretion and enhances potassium and calcium secretion. Sennoside increases paracellular permeability to small molecules, accelerates colon transit and softens fecal pellets. Sennoside can be used for the research of constipation, melanosis coli, and colorectal cancer[1][2][3].

In Vivo

Sennoside (50 mg/kg; p.o.; single dose) induces a time-dependent reversal of net H2O, Na+, and Cl− absorption to secretion in rat colon, with peak effects at 6 hours; by 12 hours, Cl− returns to net absorption, while net K+ and Ca2+ secretion increases and remains elevated through 24 hours[3].
Sennoside (50 mg/kg; p.o.; single dose) transiently elevates paracellular permeability at 6 hours, does not induce significant epithelial cell damage or alter cAMP pathway activity, and not affect Na+, K+-ATPase activity overall[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Wistar (female, ~200 g body weight)[3]
Dosage: 50 mg/kg
Administration: p.o.; single dose
Result: Showed no change in net H2O, Na+, Cl-, and K+ absorption/secretion from controls at 2 and 4 hours post-treatment.
Reversed net H2O, Na+, and Cl- absorption to net secretion at 6 hours (H2O: -0.34 mL/10 cm colon/h, Na+: -44 μmol/10 cm colon/h, Cl-: -32 μmol/10 cm colon/h; all p ≤ 0.001 vs controls).
Increased net K+ secretion to -15.3 μmol/10 cm colon/h at 6 hours (p ≤ 0.05 vs controls).
Increased net Ca2+ secretion to -1.14 μmol/10 cm colon/h at 6 hours (p ≤ 0.01 vs controls).
Increased paracellular permeability to 3-fold higher than controls at 6 hours (-336 μl/10 cm colon/h, p ≤ 0.001 vs controls).
Showed persistent but diminished net H2O and Na+ secretion at 12 hours (H2O: -0.51 mL/10 cm colon/h, Na+: -13 μmol/10 cm colon/h; both p ≤ 0.001 vs controls), while Cl- returned to net absorption (9 μmol/10 cm colon/h, p ≤ 0.001 vs controls).
Increased net K+ secretion to -22.8 μmol/10 cm colon/h at 12 hours (p ≤ 0.001 vs controls).
Increased net Ca2+ secretion to -0.97 μmol/10 cm colon/h at 12 hours (p ≤ 0.001 vs controls).
Showed persistent reduced net H2O secretion at 24 hours (-0.20 mL/10 cm colon/h, p ≤ 0.001 vs controls), while Na+ and Cl- showed net absorption (Na+: 18 μmol/10 cm colon/h, Cl-: 34 μmol/10 cm colon/h; both p ≤ 0.001 vs controls).
Increased net K+ secretion to -23.9 μmol/10 cm colon/h at 24 hours (p ≤ 0.001 vs controls).
Increased net Ca2+ secretion to -1.18 μmol/10 cm colon/h at 24 hours (p ≤ 0.001 vs controls).
Showed no significant increase in LDH leakage into the colon lumen at any time point post-treatment.
Showed unchanged Na+, K+-ATPase activity at 4 and 6 hours, with a statistically significant but inconsistent reduction at 24 hours (568 nmol Pi/mg protein/10 min, p ≤ 0.001 vs controls).
Showed unchanged colon mucosal cAMP content and phosphodiesterase activity at 6 hours post-treatment.
Clinical Trial
Molecular Weight

862.74

Formula

C42H38O20
CAS No.
SMILES

OC[C@@H](O1)[C@@H](O)[C@H](O)[C@@H](O)[C@@H]1OC2=CC=CC3=C2C(C4=C(C=C(C(O)=O)C=C4O)C3C5C6=C(C(C7=C5C=C(C(O)=O)C=C7O)=O)C(O[C@H]8[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O8)=CC=C6)=O
Structure Classification
Initial Source
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Room temperature in continental US; may vary elsewhere.
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Sennoside Related Classifications

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Keywords:

Sennoside517-43-1ApoptosisMDM-2/p53PAKCalcium Channelp21 activated kinasesCa2+ channelsCa channelsrat coloncolorectal cancerp21/WAFmelanosis colishikimate pathwayconstipationp53colonic epithelial cellsCassia angustifoliamevalonate pathwayInhibitorinhibitorinhibit

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