Aim of the Study: The aim of the present study was to explore the antitumor activity of the ethanolic extract of Albizia lebbeck L. pods against Ehrlich ascites carcinoma (EAC) in Swiss albino mice and its cytotoxic effect against HeLa and A549 cell lines in vitro. Materials and Methods: Antitumor activity of ethanolic extract of A. lebbeck L. (ALEE) pods was evaluated in Swiss albino mice against EAC cell lines at the doses of 200 and 400 mg/kg body weight which were given by intraperitoneal route of administration and was compared with 5-fluorouracil (5-FU), the reference standard. The extract and 5-FU were administered for 14 consecutive days. After 24 h of the last dose and 18 h of fasting, the mice were sacrificed and the antitumor effect of ALEE was assessed by evaluating tumor volume, viable and nonviable tumor cell count, increase in life span, and hematological parameters of EAC-bearing hosts.In vitro cytotoxicity has been assessed using (2,3-bis[2-Methoxy-4-nitro-5sulfophenyl]-2H-tetrazolium-5-carboxyanilide inner salt assay method and was compared with cisplatin, the reference standard. Results: ALEE showed direct cytotoxicity on EAC cells in a dose-dependent manner. ALEE exhibited a significant (P < 0.001) decrease in the body weight, tumor volume, viable cell count, tumor weight, and elevated the life span of EAC tumor-bearing mice. Hematological profile such as red blood cell, hemoglobin, white blood cell, and platelet count was reverted to the normal level in ALEE-treated mice. Conclusion: The results showed that the ethanolic extract of A. lebbeck L. has a powerful antitumor activity because it was effective in significantly inhibiting the tumor growth in both in vivo and in vitro cancer cell lines.

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T-helper subtype imbalance is intricate in type 1 diabetes (T1D) and asthma initiation. The role of quercetin in immune dysregulation in comorbid conditions of T1D and asthma is not available. In this study, it was thought worthy to evaluate the role of quercetin on modulating Th1/Th2 cytokine dysregulation in comorbid diabetic asthma. Male Balb/c mice were injected intravenously with alloxan (80 mg/kg) to persuade T1D. Succeeding diabetes introduction, two intraperitoneal sensitizing doses of ovalbumin emulsion (50 µg ovalbumin blended with 2.5 mg alum/sensitization) were given on days 3 and 8. Mice were given intranasal challenges of ovalbumin (100 µg ovalbumin/25 µl of sterile saline) on days 13-15. Oral quercetin treatment (10-30 mg/kg) was given daily on days 3-15. Nasal hyperresponsiveness (NHR) was recorded immediately after Ova challenge on day 16. Bronchoalveolar lavage fluid (BALF), blood, and lungs were collected 1-hour post NHR for further analysis. Quercetin treatment significantly decreased eosinophils, interleukin-4 while increasing interferon-gamma in blood, and BALF and reduced the allergic airway inflammation by inhibiting inflammatory cell infiltration and mucous cell metaplasia. Furthermore, quercetin with a dose of 30 mg/kg demonstrated a significant glucose reduction. Thus, quercetin exerted dose-dependent anti-asthma activity by modulating Th1/Th2 balance with glucose-lowering potential in comorbid mice.

Cytarabine (Ara-C) is a nucleoside analogue used in the treatment of cancers and viral infections. It has teratogenic potential and causes a variety of birth defects in fetuses. Alpha-lipoic acid (ALA) is a natural antioxidant offers protection against the developmental toxicity induced by drug- or toxicant-exposure or pathological conditions. This study was aimed at evaluating the protective effect of ALA against Ara-C induced developmental toxicity in rat fetus. Pregnant rats divided into five groups and received normal saline, ALA200 mg/kg, Ara-C12.5 mg/kg, Ara-C25 mg/kg and, Ara-C25 mg/kg plus ALA200 mg/kg respectively from gestational day (GD) 8 to GD14 and sacrificed on GD21. Ara-C treatment led to a significant and dose-dependent decrease in food intake, weight gain, placental weight, and an increase in oxidative stress in pregnant rats. Further, the in-utero exposure to Ara-C led to an increase in fetal mortality, resorptions, oxidative stress, external morphological anomalies and limb abnormalities, and impaired ossification. Co-administration of ALA resulted in amelioration of the footprints of Ara-C induced toxicity in pregnant rats as well as the fetus. These findings indicate that the ALA supplementation offers protection against developmental toxicity caused by Ara-C prenatal exposure in rats.