Maurya Harikesh, Dhiman Sheena, Dua Kamal, Gupta Gaurav
Department of Pharmacology, Siddhartha Institute of Pharmacy, Near I.T. Park, Sahastradhara Road, Dehradun, India.
School of Medicine and Public Health, University of Newcastle, Newcastle, NSW 2308, Australia.
Recent Pat Drug Deliv Formul. 2016;10(2):165-73. doi: 10.2174/1872211310666160321123610.
The present study is aimed at bringing out the information on the effect of berberine chloride in hyper and hypo thyroidal model with two dose levels.
The research article also reviewed details of various existing patents associated with comprehensive compilation regarding the therapeutic application of berberine and related forms.
Sixty female wistar rats weighing between 150-250 gm were divided in to 10 groups. The animals were grouped in to solvent control; hypothyroid; hyperthyroid; prophylactic with two different doses of berberine chloride (50 and 100 mg/kg); treatment groups similar to that of the prophylactic and therapeutic group. To substantiate the dose dependent effect of berberine chloride in 6-n-propyL-2-thiouracil (PTU) induced hypothyroidism, lipid profile, thyroid profile, enzymes profiles and blood profiles, in addition to histopathological studies were also carried out. There was no any significant difference in the lipid profile among solvent control, treatment and prophylactic groups. However, there was a significant difference (***p<0.001) in serum triglycerides, LDL and VLDL of hypothyroid group when compound to that of the rest.
As far as thyroid profile is concerned, T3 level of berberine chloride (50 mg/kg) treated groups (prophylactic+ treatment) showed a significant rise compared to hypothyroid group. TSH level in prophylactic groups was far higher than the rest of the groups (3.002±0.0192, 1.051±0.0008 against the solvent control, 0.308±0.008). SGOT, SGPT levels were significantly higher with the therapeutic group than that of the normal and hypo-thyroidal group. Blood profile of berberine chloride (100 mg/kg) treated therapeutic group was comparable to that of the solvent control than all other groups. The probable mechanism underlying may be that inactivation of type I 5.-iodothyronine deiodinase (5.DI) enzyme by NF-kB pathway.
From the findings of the current study it can be concluded that berberine chloride possesses both thyroid stimulating and suppressing activities depending on its dose, especially berberine chloride 50 mg/kg supports thyroid stimulating property.
本研究旨在揭示两种剂量水平的盐酸小檗碱对甲状腺功能亢进和减退模型的影响信息。
该研究文章还回顾了与小檗碱及其相关形式的治疗应用综合汇编相关的各种现有专利的细节。
将60只体重在150 - 250克之间的雌性Wistar大鼠分为10组。动物被分为溶剂对照组；甲状腺功能减退组；甲状腺功能亢进组；用两种不同剂量的盐酸小檗碱（50和100毫克/千克）进行预防组；与预防组和治疗组类似的治疗组。为了证实盐酸小檗碱在6 - n - 丙基 - 2 - 硫氧嘧啶（PTU）诱导的甲状腺功能减退中的剂量依赖性作用，除了组织病理学研究外，还进行了血脂谱、甲状腺谱、酶谱和血液谱分析。溶剂对照组、治疗组和预防组之间的血脂谱没有任何显著差异。然而，与其他组相比，甲状腺功能减退组的血清甘油三酯、低密度脂蛋白和极低密度脂蛋白存在显著差异（***p<0.001）。
就甲状腺谱而言，盐酸小檗碱（50毫克/千克）治疗组（预防 + 治疗）的T3水平与甲状腺功能减退组相比有显著升高。预防组的促甲状腺激素水平远高于其他组（3.002±0.0192，1.051±0.0008，而溶剂对照组为0.308±0.008）。治疗组的谷草转氨酶、谷丙转氨酶水平显著高于正常组和甲状腺功能减退组。盐酸小檗碱（100毫克/千克）治疗组的血液谱与溶剂对照组相比，优于所有其他组。潜在的可能机制可能是I型5 - 碘甲状腺原氨酸脱碘酶（5 - DI）通过核因子κB途径失活。
从当前研究的结果可以得出结论，盐酸小檗碱根据其剂量具有甲状腺刺激和抑制活性，特别是50毫克/千克的盐酸小檗碱具有甲状腺刺激特性。
